Chapter 46 NURSING MANAGEMENT: acute kidney injury and chronic kidney disease

1. Differentiate between acute kidney injury and chronic kidney disease.

2. Identify criteria used in the classification of acute kidney injury using the acronym RIFLE (risk, injury, failure, loss, end-stage kidney disease).

3. Describe the clinical course of reversible acute kidney injury.

4. Explain the multidisciplinary care and nursing management of a patient with acute kidney injury.

5. Define chronic kidney disease and delineate the five stages of chronic kidney disease based on the glomerular filtration rate.

6. Select risk factors that contribute to the development of chronic kidney disease.

7. Summarise the significance of cardiovascular disease in individuals with chronic kidney disease.

8. Explain the conservative multidisciplinary care for and the related nursing management of the patient with chronic kidney disease.

9. Differentiate between kidney replacement options for individuals with end-stage kidney disease.

10. Compare and contrast nursing interventions for individuals on peritoneal dialysis and haemodialysis.

11. Discuss the nursing role in the management of individuals who receive a kidney transplant.

Renal insufficiency is the partial or complete impairment of kidney function resulting in an inability to excrete metabolic waste products and water, as well as functional disturbances of all body systems. Renal insufficiency is classified as acute or chronic (see Table 46-1). Acute kidney injury (AKI) has a rapid onset. Although AKI is potentially reversible, despite advances in treatment over the last 30 years¹ the mortality rate for AKI remains high, particularly for patients requiring intensive care.

TABLE 46-1 Comparison of acute kidney injury and chronic kidney disease

	Acute kidney injury	Chronic kidney disease
Onset	Sudden	Gradual, often over many years
Most common cause	Acute tubular necrosis	Diabetic nephropathy
Diagnostic criteria	Acute reduction in urine output and/or elevation in serum creatinine	GFR <60 mL/min/1.73m² for >3 months and/or kidney damage >3 months
Reversibility	Potentially	Progressive and irreversible
Mortality	High (about 60%)	19–24% (patients on dialysis)
Primary cause of death	Infection	Cardiovascular disease

GFR, glomerular filtration rate.

Source: Kellum J, Bellomo R, Ronco C. Definition and classification of acute kidney injury. Nephron Clin Pract 2008; 109:4. United States Renal Data System, 2009.

Chronic kidney disease (CKD) is often a silent disease that develops slowly over months to years and, for a relatively small number of people, can necessitate the initiation of kidney replacement therapy (dialysis or transplantation) for long-term survival. CKD is a manageable chronic disease that requires long-term and often life-long care. People with CKD are also at risk of having an acute episode of renal insufficiency on top of the underlying CKD; this is termed acute-on-chronic kidney disease. Long-term treatment of CKD is a result of technical advances, improved surgical techniques and more effective immunosuppressive therapy, and the collaboration of professionals and industry leaders whose efforts are changing the outcomes of patients with CKD.

Acute kidney injury

Acute kidney injury, previously known as acute renal failure, is the term used to encompass the entire range of the syndrome from very slight deterioration in kidney function to severe impairment. AKI is characterised by a rapid loss of kidney function demonstrated by a rise in serum creatinine and/or a reduction in urine output. The severity of dysfunction can range from a small increase in serum creatinine or reduction in urine output to the development of azotaemia (an accumulation of nitrogenous waste products [urea nitrogen, creatinine] in the blood) severe enough to warrant kidney replacement therapy (KRT). There are also significant changes to electrolytes and fluid status as well as acid–base status. The nursing care of AKI is challenging, since the patient is often critically ill and requires constant monitoring as the clinical situation can alter rapidly.²

Uraemia is the condition in which renal function declines to the point that symptoms develop in multiple body systems. AKI is often associated with oliguria, which is a decrease in urinary output to less than 400 mL per day. In about 50% of cases there is normal or increased urinary output (non-oliguria). Patients with non-oliguria usually have fewer complications and recover more quickly.²

AKI usually develops over hours or days with progressive elevations of serum urea, creatinine and potassium levels with or without oliguria. AKI usually affects people with other life-threatening conditions (see Table 46-2).² Most commonly, AKI follows severe, prolonged hypotension or hypovolaemia, or exposure to a nephrotoxic agent. Approximately 5–7% of all hospitalised patients are affected, as are an estimated 35–65% of critically ill patients.³ Older adults have a higher incidence of developing AKI, most likely due to increased diagnostic procedures and treatment with nephrotoxic agents, as well as the increased likelihood of already having some degree of pre-existing renal insufficiency. The acronym RIFLE (risk, injury, failure, loss, end-stage kidney disease) is used to classify the severity (R, I, F) and outcome (L, E), as well as the amount of urine output and the increase in serum creatinine. This classification system facilitates the early diagnosis of AKI. The Acute Kidney Injury Network (AKIN) has modified the RIFLE criteria, renaming the stages as stages 1, 2 and 3, with stage 3 patients requiring KRT.⁴ Both classifications are shown in Table 46-3.

TABLE 46-2 Common causes of acute kidney injury

ACE, angiotensin-converting enzyme; CMV, cytomegalovirus; GI, gastrointestinal.

TABLE 46-3 Classification/staging systems for acute kidney injury

AKIN, acute kidney injury network; RIFLE, risk, injury, failure, loss, end-stage kidney disease; SCr, serum creatinine; UOP, urine output.

Source: Dennen P, Douglas IS, Anderson R. Acute kidney injury in the intensive care unit: an update and primer for the intensivist. Critical Care Med 2010; 38(1):261–275.

AETIOLOGY AND PATHOPHYSIOLOGY

The causes of AKI are multiple and complex, with the most common being ischaemia (due to hypotension) or exposure to nephrotoxic agents. The causes of AKI are commonly categorised as prerenal (55–60%), intrarenal (or intrinsic; 35–40%) and postrenal (<5%) (see Table 46-2 and Fig 46-1).^5,⁶

Figure 46-1 Prerenal, intrarenal and postrenal causes of acute kidney injury.

Prerenal AKI is caused by factors external to the kidneys that reduce systemic circulation, causing a reduction in renal blood flow, and lead to decreased glomerular perfusion and filtration.⁶ Hypovolaemia, decreased cardiac output, decreased peripheral vascular resistance and vascular obstruction all can decrease the effective circulating volume of the blood to the kidneys, resulting in glomerular hypoperfusion. Oliguria occurs as the kidneys respond to the decreased blood flow by activating the renin–angiotensin–aldosterone system. This is due to an autoregulatory response by the afferent and efferent arterioles in an attempt to restore renal blood flow. As a result, the kidneys conserve sodium and water. Decreased renal perfusion also decreases clearance of wastes (azotaemia). As decreased perfusion continues, the kidneys lose their ability to engage in compensatory mechanisms and intrarenal damage to renal tissue occurs. Reduced ability to compensate for the hypoperfusion results in lower urine output due to the kidneys’ inability to excrete water, a rise in serum urea and creatinine levels proportional to each other (ratio of >10:1), and the inability of the kidneys to conserve sodium.

The causes of intrarenal AKI include conditions that cause direct damage to the kidney tissue (parenchyma), resulting in impaired nephron function.⁶ The damage by intrarenal causes usually results from prolonged ischaemia (prolonged prerenal AKI), nephrotoxins, haemoglobin released from haemolysed red blood cells (RBCs) or myoglobin released from necrotic muscle cells. A nephrotoxin can cause obstruction of intrarenal structures by crystallisation or actual damage to the epithelial cells of the tubules. Rhabdomyolysis is caused by the release of haemoglobin and myoglobin, which block the tubules and cause renal vasoconstriction. Primary renal diseases such as acute glomerulonephritis and systemic lupus erythematosus may also cause AKI.

Acute tubular necrosis (ATN) is the most common cause of intrarenal AKI caused by prolonged glomerular ischaemia, nephrotoxins or pigments (see Fig 46-2).^6,⁷ Ischaemic and nephrotoxic ATN are responsible for 90% of intrarenal AKI cases. Patients more prone to developing ischaemic ATN include those who have experienced severe hypovolaemia, major surgery, trauma or burns or the development of sepsis.⁶ Regardless of the cause of ischaemia, if it lasts for longer than 2 hours then there is a disruption in the glomerular basement membrane structure and patchy destruction of the tubular epithelium.⁸ Common nephrotoxic agents associated with ATN include aminoglycoside antibiotics, contrast media and non-steroidal anti-inflammatory drugs (NSAIDS). Nephrotoxic agents cause necrosis of the tubular epithelial cells, which slough off and plug the tubules, but usually leave the basement membrane intact (see Fig 46-3). The risk for ATN is higher when nephrotoxic agents are given to older people or those with pre-existing CKD.^7,⁹ ATN is potentially reversible if the basement membrane is not destroyed and the tubular epithelium regenerates.

Figure 46-2 Acute tubular necrosis. In acute tubular necrosis, the kidneys are swollen and pale.

Figure 46-3 Nephron destruction in acute kidney injury. A, Normal nephron. B, Damage from renal ischaemia results in patchy necrosis of the tubule. The lumen may be blocked by casts. C, Damage from nephrotoxic agents.

Possible pathological processes involved in ATN include the following:

1. Hypovolaemia and decreased renal blood flow stimulate renin release, which activates the renin–angiotensin–aldosterone system and results in constriction of the peripheral arteries and the renal afferent arterioles. With decreased renal blood flow, a decreased glomerular capillary pressure and glomerular filtration rate (GFR) result, as well as tubular dysfunction and oliguria.

2. Ischaemia alters glomerular epithelial cells and decreases glomerular capillary permeability. This reduces the GFR, which significantly reduces blood flow and leads to tubular dysfunction.

3. When tubules are damaged, interstitial oedema occurs, and necrotic epithelial cells accumulate in the tubules. The debris lowers the GFR by obstructing the tubules and increasing intratubular pressure.

4. Glomerular filtrate leaks back into plasma through holes in the damaged tubular membranes, which decreases intratubular fluid flow.

Postrenal AKI involves a mechanical obstruction of urinary outflow.⁸ As the flow of urine is obstructed, urine refluxes into the renal pelvis, impairing kidney function. The most common causes are benign prostatic hyperplasia, prostate cancer, calculi, trauma and extrarenal tumours. Postrenal causes of AKI account for less than 5% of cases. Postrenal AKI is almost always treatable if identified before permanent kidney damage occurs. Bilateral ureteral obstruction leads to hydronephrosis (kidney dilation), an increase in hydrostatic pressure and tubular blockage, resulting in a progressive decline in kidney function. Unilateral obstruction rarely results in azotaemia and if bilateral obstruction is relieved within 48 hours of onset, it is likely that complete recovery of GFR can be achieved; after 12 weeks recovery is unlikely. Prolonged obstruction can lead to tubular atrophy and irreversible kidney fibrosis.¹⁰

CLINICAL COURSE

Prerenal and postrenal situations that have not yet resulted in intrarenal damage usually resolve quickly with correction of the cause. However, if parenchymal damage has occurred due to either prerenal or postrenal causes, or when parenchymal damage occurs directly, as with ATN or other intrarenal causes, AKI occurs and has a prolonged course of recovery. Clinically, AKI may progress through four phases: initiating, maintenance, diuretic and recovery. In some situations, the patient does not recover from AKI and CKD results, eventually requiring dialysis or a kidney transplant.^6,¹¹

Initiating phase

This begins at the time of the insult and continues until the signs and symptoms become apparent. It can last hours to days.

Maintenance phase

The most common initial manifestation of AKI is oliguria caused by a reduction in the GFR. Oliguria usually occurs within 1–7 days of the causative event. If the cause is ischaemia, oliguria may occur within 24 hours. When nephrotoxic drugs are involved, the onset may be delayed for as long as a week. About 50% of patients will not demonstrate oliguria (often called non-oliguric AKI), making the initial diagnosis more difficult.⁹ The duration of the maintenance phase is, on average, about 10–14 days, but can be months in some cases. The longer the maintenance phase lasts, the poorer the prognosis for recovery of complete renal function.

It is important to distinguish prerenal oliguria from the oliguria of intrarenal AKI (see Table 46-4).¹⁰ In prerenal oliguria there is no damage to the renal tissue. The oliguria is caused by a decrease in circulating blood volume (e.g. as a result of severe dehydration, decreased cardiac output, burns) and is usually reversible following the administration of sufficient quantities of intravenous fluids. Volume resuscitation can correct prerenal conditions resulting from absolute or relative hypovolaemia. However, renal hypoperfusion resulting from low cardiac output (e.g. end-stage congestive heart failure) and reduced renal perfusion pressure (e.g. sepsis or liver failure) cannot always be corrected by fluid administration.¹⁰ With a decrease in circulating blood volume, autoregulatory mechanisms that increase angiotensin II, aldosterone, noradrenaline and antidiuretic hormone (ADH) attempt to preserve blood flow to essential organs. Vasoconstriction occurs along with sodium and water retention. Prerenal oliguria is characterised by urine with a high specific gravity (>1.015) and a low sodium concentration (<10–20 mmol/L).

TABLE 46-4 Comparison of prerenal oliguria with oliguria of acute kidney injury

	Prerenal oliguria	Oliguria of acute kidney injury
Urine output	Low	Low
Serum urea level	Elevated	Elevated
Serum creatinine level	Normal or slightly elevated	Elevated
Urine specific gravity	High	Fixed at 1.010
Urine sodium level	Low	High

In contrast, oliguria of intrarenal AKI is characterised by urine with a normal specific gravity (1.010) and a high sodium concentration (>40 mmol/L), indicating that the injured tubules cannot respond to autoregulatory mechanisms. In addition, the oliguria of intrarenal AKI caused by ATN from ischaemia or toxins is characterised by the presence of tubular RBC and white blood cell (WBC) casts in the urine. The casts are formed from mucoprotein impressions of the necrotic renal tubular epithelial cells, which detach or slough into the tubules.

In addition to oliguria, other changes during the maintenance phase include fluid and electrolyte abnormalities, and uraemia. The nurse must be alert for the signs and symptoms of these changes.

Eventually all body systems become involved in the uraemia of AKI (see Table 46-5). The extrarenal manifestations are generally similar to those found in the patient with chronic uraemia, discussed later in this chapter.

TABLE 46-5 Manifestations of acute kidney injury

Diuretic phase

The diuretic phase begins with a gradual increase in daily urine output to 1–3 L per day but may reach 3–5 L or more. Although urine output is increasing, the nephrons are still not fully functional. The high urine volume is caused by osmotic diuresis as a result of the high urea concentration in the glomerular filtrate and the inability of the tubules to concentrate the urine. In this phase the kidneys have recovered their ability to excrete wastes but not to concentrate the urine. Hypovolaemia and hypotension can occur due to massive fluid losses. Patients who develop an oliguric phase will have greater diuresis than patients without oliguria.

At this stage the uraemia may still be severe, as reflected by low creatinine clearances, elevated serum creatinine and urea levels, and persistent signs and symptoms. Because of the large losses of fluid and electrolytes, the patient must be monitored for hyponatraemia, hypokalaemia and dehydration. The diuretic phase may last 1–3 weeks. Near the end of this phase the patient’s acid–base, electrolyte and waste product (urea, creatinine) values begin to normalise.

Recovery phase

The recovery phase begins when the GFR increases, allowing the serum urea and creatinine levels to plateau and then decrease. The tubular cells undergo a process of repair and regeneration. Although the major improvements occur in the first 1–2 weeks of this phase, kidney function may take up to 12 months to stabilise.

The outcome of AKI is influenced by the patient’s overall health, the severity of kidney failure, and the number and type of complications. Some individuals do not recover and progress to CKD.¹¹ Older patients are less likely to recover full kidney function than younger patients. Among the individuals who recover, the majority achieve clinically normal kidney function with no complications.¹²

DIAGNOSTIC STUDIES

A thorough history is essential for diagnosing the aetiology of AKI. Prerenal causes should be considered when there is a history of dehydration, blood loss or severe heart disease. Intrarenal causes may be suspected if the patient has been taking or has been administered potentially nephrotoxic drugs or has a recent history of prolonged hypotension or hypovolaemia. Postrenal AKI is suggested by a history of changes in urinary stream, stones, benign prostatic hyperplasia or cancer of the bladder or prostate.

Although changes in urine output and serum creatinine occur relatively late in the course of AKI, there are no better criteria for a diagnosis of AKI. An increase in serum creatinine may not be evident until there is a loss of more than 50% of kidney function. The rate of increase in serum creatinine is also very important as a diagnostic indicator and in determining the severity of injury.

Urinalysis is an important diagnostic test. Urine sediment containing abundant cells, casts or proteins suggests intrarenal disorders. The urine osmolality, sodium content and specific gravity help in differentiating the causes of AKI. Urine sediment may be normal in both prerenal and postrenal AKI. Haematuria, pyuria and crystals may be seen with postrenal AKI.

To establish a diagnosis of AKI, other testing may be required. Serum creatinine and urea are used to evaluate kidney function. In AKI, serum creatinine levels rapidly increase, often within 24–48 hours. The estimated glomerular filtration rate (eGFR) is an inaccurate marker of kidney function in AKI but it does provide an estimate, based on the serum levels, of how well the kidneys are functioning. The best test of kidney function is the 24-hour urine collection, which can be inconvenient for patients—hence why the eGFR was developed. In Australia, the eGFR is reported with every request for serum creatinine in adults. New serum and urine biomarkers are being developed to assist in the early diagnosis of AKI.⁶ A renal ultrasound is often the first test done since it provides imaging without exposure to potentially nephrotoxic contrast agents. It is useful for evaluating possible kidney disease and obstruction of the urinary collecting system. A renal scan can assess renal blood flow and the integrity of the collecting system. A computed tomography (CT) scan and magnetic resonance imaging (MRI) can identify lesions and masses, collections, obstructions and vascular anomalies.

MULTIDISCIPLINARY CARE

Because AKI is potentially reversible, the primary goals of treatment are to eliminate the cause, manage the signs and symptoms, and prevent complications while the kidneys recover (see Box 46-1). The initial assessment of patients with AKI classically includes the differentiation between prerenal, intrarenal and postrenal causes.¹⁰ The first step is to determine whether there is adequate intravascular volume and cardiac output to ensure adequate perfusion of the kidneys. Volume resuscitation is vital in the management of prerenal AKI, with the first choice usually being crystalloids (e.g. normal saline), along with colloids or blood as necessary later. The goal is to restore renal perfusion, reduce ischaemic time and prevent the development of intrinsic renal failure.^7,¹⁰ It can be challenging to re-establish effective renal perfusion in patients with volume redistribution from the intravascular space (e.g. burns, congestive heart failure). Renal dose dopamine does not improve renal perfusion and should be avoided.⁶ The use of loop diuretics (e.g. frusemide) in the deterrence and treatment of AKI is not recommended; however, diuretics are often used in oliguric AKI in an attempt to alter it to non-oliguric AKI.^9,¹³ If AKI is already established, forcing fluids and diuretics will not be effective and may, in fact, be harmful. Nephrotoxic agents are avoided throughout the course of AKI. Conservative therapy may be all that is necessary until renal function improves, although intensive care patients with AKI often require renal replacement therapy.^6,¹⁰ The general trend is to initiate early and frequent dialysis to minimise symptoms and prevent complications.

BOX 46-1 Acute kidney injury

MULTIDISCIPLINARY CARE

^*See Box 46-2.

^†Renal formulations of these two forms of nutrition are available.

Fluid intake must be closely monitored during the maintenance phase. The general rule for calculating the fluid restriction is to add all losses for the previous 24 hours (e.g. urine, diarrhoea, emesis, blood) plus 600 mL for insensible losses (e.g. respiration, diaphoresis). For example, if a patient excreted 300 mL of urine on Tuesday with no other losses, the fluid intake restriction on Wednesday would be 900 mL (including oral and intravenous fluids). Daily weight, strict fluid balance charts and measurement of haemodynamic parameters are useful indicators of fluid status.

Hyperkalaemia is one of the most serious complications in AKI because it can cause life-threatening cardiac arrhythmias. The various therapies used to treat elevated potassium levels are listed in Box 46-2. Both insulin and sodium bicarbonate temporarily shift potassium into the cells but it will eventually shift back out. Calcium gluconate raises the threshold at which arrhythmias will occur. Only sodium (or calcium) polystyrene sulfonate (Resonium) and dialysis actually remove potassium from the body. Sodium (or calcium) polystyrene sulfonate can be administered orally or rectally. If administered orally, an aperient should also be administered to avoid constipation. Oral polystyrene sulfonate should never be given to a patient with a paralytic ileus, because bowel necrosis can occur.

BOX 46-2 Therapies to treat elevated potassium levels

1. Regular insulin administration IV

Potassium moves into the cells when insulin is given. Glucose is given concurrently to prevent hypoglycaemia. When the effects of insulin diminish, potassium shifts back out of the cells.

2. Sodium bicarbonate

Therapy can correct acidosis and causes shift of potassium into the cells.

3. Calcium gluconate IV

Therapy is given IV and generally used in advanced cardiac toxicity. Calcium raises the threshold for excitation, which causes arrhythmias.

4. Dialysis

Haemodialysis can bring potassium levels to normal within 30 min to 2 h.

5. Sodium or calcium polystyrene sulfonate (resonium)

Cation-exchange resin is administered by mouth or retention enema. When resin is in the bowel, potassium is exchanged for sodium. Therapy removes 1 mmol of potassium per gram of drug. A laxative is often administered concurrently to prevent severe constipation and to allow for evacuation of potassium-rich stool from body.

6. Dietary restriction

Daily potassium intake is limited to 40 mmol.

IV, intravenous.

The most common indications for dialysis in AKI include: (1) volume overload, resulting in compromised cardiac and/or pulmonary status; (2) elevated potassium level with ECG changes; (3) metabolic acidosis (serum bicarbonate level <15 mmol/L); (4) serum urea level greater than 20 mmol/L; (5) significant change in mental status; and (6) pericarditis, pericardial effusion or cardiac tamponade. Laboratory values provide rough parameters, and clinical assessment is the most important guide in determining the need for dialysis.

Continuous renal replacement therapy (CRRT) is used in the treatment of AKI in the critical care or high dependency setting. (CRRT is discussed on p 1322.) In the haemodynamically unstable patient, CRRT provides gradual removal of excess fluid and solutes. It is technically similar to haemodialysis (HD) and requires extracorporeal blood circulation via cannulation of two veins or an artery and a vein. Blood removed from the artery or vein passes through a haemofilter where excess solutes and water are removed and then the blood is returned to the patient. CRRT runs continuously and requires at least 12–24 hours to accomplish what can be done with 3–4 hours of HD. Larger amounts of fluid may be removed than with intermittent HD. It is the preferred treatment in the haemodynamically unstable patient with mild-to-moderate AKI and with severe fluid overload.

Other dialysis options available for AKI are HD and peritoneal dialysis (PD). HD is the method of choice when rapid changes are required in a short period of time. It is technically more complicated because specialised staff and equipment and vascular access are required. Anticoagulation therapy may be necessary to prevent blood from clotting when the blood contacts the foreign membrane material in the dialysis blood circuit. Rapid fluid shifts during HD may cause hypotension. HD is preferred for the hypercatabolic patient and for the individual who has had abdominal or thoracic trauma or surgery. PD is much simpler than HD, although rarely used as it carries the risk of peritonitis, is less efficient in the catabolic patient and requires longer treatment times. PD may be preferred for the individual with intracranial bleeding or cardiovascular instability or when HD is unavailable. (HD and PD are discussed on pp 1317 and 1314, respectively.)

Nutritional therapy

The challenge of nutritional management in AKI is to provide adequate kilojoules to prevent catabolism despite the restrictions required to prevent electrolyte and fluid disorders and azotaemia. If the patient does not receive adequate nutrition, catabolism of body protein will occur.^14,¹⁵ This process causes increased urea, phosphate and potassium levels. Early referral to a dietician is essential to maintaining an adequate nutritional status. Adequate energy should be primarily from carbohydrate and fat sources to prevent ketosis from endogenous fat breakdown and gluconeogenesis from muscle protein breakdown. The daily kilojoule intake should be about 125–150 kJ/kg. Protein intake is generally 1.5 g/kg but can be as high as 2 g/kg if the patient is catabolic and receiving CRRT.¹⁴ Essential amino acid supplements can be given for amino acid and kilojoule supplementation.

Specialty formulations lower in certain electrolytes (i.e. phosphate, potassium and sodium) than standard products may be beneficial in the intensive care patient with AKI.¹⁴ Potassium and sodium are regulated in accordance with plasma levels. Sodium is restricted as needed to prevent oedema, hypertension and heart failure. Dietary fat intake is increased so that the patient receives at least 30–40% of total kilojoules from fat. Fat emulsion intravenous (IV) infusions can also be given as a nutritional supplement and provide a good source of non-protein kilojoules (see Ch 39). If a patient cannot maintain adequate oral intake, enteral nutrition is the preferred route for nutritional support. When the GI tract is not functional, total parenteral nutrition is necessary for the provision of adequate nutrition. The patient treated with total parenteral nutrition may need CRRT or daily HD to remove the excess fluid. Concentrated formulas are available to minimise fluid volume.

NURSING MANAGEMENT: ACUTE KIDNEY INJURY

Nursing assessment

An assessment of the patient with AKI includes the specific areas presented in Table 46-5. It is important to frequently and accurately monitor the vital signs and intake and output. The urine should be examined for colour, specific gravity, glucose, protein, blood or sediment. The patient’s general appearance should be assessed, including skin colour, peripheral oedema, neck vein distension and bruises.

If the patient is receiving dialysis, the access site should be observed for signs of inflammation. The patient’s mental status and level of consciousness should also be evaluated. The oral mucosa should be examined for dryness and inflammation. The lungs should be auscultated for crackles and rhonchi or diminished breath sounds. The heart should be monitored for the presence of an S₃ heart sound, other murmurs or a pericardial friction rub. ECG readings should be assessed for the presence of arrhythmias. Laboratory values and diagnostic test results should be reviewed. All of the previous data are essential for developing a collaborative plan of care.

Planning

The overall goals are that the patient with AKI will: (1) completely recover without any loss of kidney function; (2) be maintained in normal fluid and electrolyte balance; (3) have decreased anxiety; and (4) comply with and understand the need for careful follow-up care.

Nursing implementation

Health promotion

Prevention of AKI is essential because of the high mortality rate and is primarily directed towards identifying and monitoring high-risk populations, controlling exposure to nephrotoxic drugs and industrial chemicals, and preventing prolonged episodes of hypotension and hypovolaemia. In the hospital, the factors that increase the risk for developing AKI are the presence of pre-existing chronic kidney disease, advanced age, massive trauma, major surgical procedures, extensive burns, cardiac failure, sepsis, obstetric complications or baseline renal insufficiency caused by hypertension or diabetes mellitus. Careful monitoring of intake and output and fluid and electrolyte balances is essential. The nurse should assess and record extrarenal losses of fluid from vomiting, diarrhoea and haemorrhage and increased insensible losses. Prompt replacement of significant fluid losses will help prevent ischaemic tubular damage associated with trauma, burns and extensive surgery. Intake and output records and the patient’s weight provide valuable indicators of fluid volume status. Aggressive diuretic therapy for the patient with fluid overload resulting from any cause can lead to inadequate renal vascular perfusion.

Streptococcal infections must be identified and treated with antibiotics. Compliance with the antibiotic regimen is critical to eliminate the source of infection and prevent complications such as acute post-streptococcal glomerulonephritis and rheumatic heart disease.

For the older adult or diabetic patient who is undergoing diagnostic studies requiring IV contrast media, special attention must be given to prevent a nephrotoxic injury secondary to the dye. Evidence shows that in patients with renal insufficiency (GFR <60 mL/min) who receive adequate hydration prior to and following the radiocontrast media procedure there is a reduced risk of developing contrast-induced nephropathy.¹⁶ Acetylcysteine together with sodium bicarbonate has been demonstrated to reduce the risk of AKI, but further research is warranted to support this practice.¹⁶ It is recommended that NSAIDs, calcineurin inhibitors, high-dose loop diuretics, aminoglycosides and other nephrotoxic agents are not administered for several days before contrast exposure to reduce the risk of developing AKI.¹⁶

Patients with urinary tract infections need prompt treatment and careful follow-up care. Chemotherapeutic drugs that cause hyperuricaemia can also put a patient at risk of AKI.

Patients who are taking drugs that are potentially nephrotoxic must have their kidney function monitored. Nephrotoxic drugs should be used sparingly in high-risk patients. When these drugs must be used, they should be given in the smallest effective doses for the shortest possible period. Patients should be cautioned about the use of over-the-counter analgesics (especially NSAIDs) because some of these may worsen kidney function in patients with borderline renal insufficiency by decreasing glomerular pressure. Angiotensin-converting enzyme (ACE) inhibitors can also decrease renal perfusion pressure and cause hyperkalaemia. Industrial and agricultural chemicals and products (organic solvents, insecticides, cleaning agents) must be monitored regularly to assess their safety for employees and the general population.

Acute intervention

The patient with AKI is critically ill and suffers not only from the effects of renal insufficiency but also from the effects of coexisting diseases or conditions (e.g. diabetes mellitus, cardiovascular disease) that also affect kidney function. The nurse must focus on the patient as a total person with many physical and emotional needs. Usually the changes caused by AKI come on suddenly. Both the patient and the family need assistance in understanding that the functioning of the whole body can be disrupted by renal insufficiency but that these changes are generally reversible with time.

The nurse has an important role in managing fluid and electrolyte balances during the maintenance and diuretic phases. Observing and recording accurate intake and output are essential. Daily weights measured with the same scale at the same time each day allow the evaluation and detection of excessive gains or losses of body fluid (1 kg is equivalent to 1000 mL of fluid). The nurse must be knowledgeable about the common signs and symptoms of hypervolaemia (in the maintenance phase) and hypovolaemia (in the diuretic phase), potassium and sodium disturbances and other electrolyte imbalances that may occur in AKI. Hyperkalaemia is a leading cause of death in the maintenance phase. Most typically, hyperkalaemia is manifested by arrhythmias and impairment of neuromuscular function, including muscle weakness, abdominal cramps, flaccid paralysis and absence of deep tendon reflexes. Cardiac conduction abnormalities to watch for include a prolonged PR interval, prolonged QRS interval, peaked T wave and depressed ST segment.

Gerontological considerations: acute kidney injury

Older adults are more susceptible to AKI than younger adults because the number of functioning nephrons decreases with age.¹⁷ Impaired function of other organ systems, such as cardiovascular disease or diabetes mellitus, can increase the risk of developing AKI. The ageing kidney is less able to compensate for changes in fluid volume, solute load and cardiac output. Common causes of AKI in older adults include dehydration, hypotension, diuretic therapy, aminoglycoside therapy, obstructive disorders (e.g. prostatic hyperplasia), surgery, infection and radiocontrast agents.

The overall prognosis after an episode of AKI is generally worse in older adults, with a mortality rate at least 25% higher than that of younger adults.¹⁷ The higher mortality rate usually results from infection, GI haemorrhage or myocardial infarction. Research continues to determine what treatment is most appropriate for older adults to decrease their mortality rate. Several studies indicate that serum cystatin C, a non-glycosolated protein produced by nucleated cells, is a better indicator of renal function than serum creatinine levels. As a result, it shows promise as a more accurate predictor of mortality risk in older adults from all causes, particularly cardiovascular disease.^17,¹⁸

Since infection is the leading cause of death overall in AKI, meticulous use of aseptic technique is critical.^2,⁶ The patient should be protected from other individuals with infectious diseases. The nurse should be alert for local manifestations of infection (e.g. swelling, redness, pain) and systemic manifestations (e.g. malaise, leucocytosis), because an elevated temperature may not be present. Patients with kidney failure have a blunted febrile response to infection (e.g. pneumonia). If antibiotics are used to treat an infection, the type, frequency and dosage must be carefully considered because the kidneys are the primary route of excretion for many antibiotics. Nephrotoxic drugs should not be used unless there is no other alternative.

Respiratory complications, especially pneumonitis, can be prevented. Measures the nurse can implement to help maintain adequate respiratory ventilation include humidified oxygen and incentive spirometry, coughing, turning and deep breathing, and ambulation.

Skin care and measures to prevent pressure ulcers should be performed because the patient usually develops oedema as well as decreased muscle tone. Mouth care is important to prevent stomatitis, which develops when ammonia (produced by bacterial breakdown of urea) in saliva irritates the mucous membranes.

Ambulatory and home care

Recovery from AKI is highly variable and depends on the underlying illness, the general condition and age of the patient, the length of the maintenance phase and the severity of nephron damage. Good nutrition, rest and activity are necessary. The diet should be high in kilojoules. Protein and potassium intake should be regulated in accordance with kidney function. Follow-up care and regular evaluation of kidney function are necessary. The patient should be taught the signs and symptoms of recurrent kidney disease. Measures to prevent the recurrence of AKI must be emphasised.

The long-term convalescence period of 3–12 months may cause psychosocial and financial hardships for the family, and appropriate counselling, social work and community health referrals should be made as indicated. If the kidneys do not recover, the patient will eventually need to transition to life on chronic dialysis or possible future transplantation.

Chronic kidney disease

Chronic kidney disease is acknowledged to represent a growing worldwide healthcare burden. CKD involves progressive, irreversible loss of kidney function and a decrease in the GFR. It is defined as either the presence of kidney damage or a GFR <60 mL/min/1.73 m² for >3 months. Kidney damage is defined as either pathological abnormalities, or markers, of damage, including abnormalities in blood or urine tests or imaging studies. Normal GFR is about 125 mL/min and is reflected by urine creatinine clearance measurements. Disease staging based on the decreased GFR is shown in Table 46-6. The vast majority of individuals with CKD stages 2–3 live normal, active lives, whereas others may progress to stages 4 and 5. Stage 5 is also called end-stage kidney disease (ESKD) and occurs when the GFR is less than 15 mL/min. At this point, KRT (dialysis or transplantation) is required.

TABLE 46-6 Stages of chronic kidney disease

CVD, cardiovascular disease; GFR, glomerular filtration rate.

Source: National Kidney Foundation.

Although there are many different causes of CKD, in Australia and New Zealand the leading causes are diabetes mellitus, glomerulonephritis and hypertension. Regardless of the cause, the end result is a systemic disease involving every body organ. (Diseases of the renal system that affect the kidney are discussed in Ch 45.)

The kidneys have remarkable functional reserve. Up to 80% of the GFR (reflected in creatinine clearance measurements) may be lost with few obvious changes in the functioning of the body. A person is born with about 2 million nephrons and can survive without dialysis until almost 90% of the nephrons are lost. In the majority of cases the individual passes through the early stages of CKD without recognising the disease state, because the remaining nephrons hypertrophy to compensate. The disease process is preventable and treatable. The prognosis and course of CKD are highly variable depending on the aetiology, the patient’s condition and age, and the adequacy of medical follow-up.

In the early stages of CKD, polyuria results from the decreased ability of the kidneys to concentrate urine. This is most noticeable at night, and the patient must arise several times to urinate (nocturia). During stage 3, when about 50% of nephron function has been destroyed, hypertension, elevated urea and creatinine levels and anaemia develop. As CKD progresses, the complications manifest, usually around late stage 3 and stage 4. These complications are a result of anaemia, electrolyte imbalances and abnormal bone and mineral metabolism. In stage 5 oedema, worsening electrolyte imbalances, metabolic acidosis and multisystem effects of uraemia develop.¹⁹

It has been estimated that as many as one in seven Australians aged 25 years and over have some degree of CKD.²⁰ The major risk factors include age, being male and ethnicity. Other risk factors, which are common in the Australian and New Zealand populations, include behavioural factors such as smoking and biomedical factors such as high blood pressure and obesity. Progression of CKD can often be slowed by controlling these modifiable risk factors and by improving disease treatment and management.²¹ CKD contributed to 15% (nearly 1.2 million) of all hospitalisations in Australia during 2007–2008, one million of which were for regular dialysis.²¹ The number of people receiving treatment for ESKD increased by 44% between 2000 and 2007, with the leading causes being diabetes mellitus and glomerulonephritis (see Fig 46-4).²² It has been estimated that one in every two people with diabetes will develop CKD.²³ The impact of CKD on the healthcare sector is substantial and growing rapidly.

Figure 46-4 Incidence of primary renal disease in Australia and New Zealand leading to end-stage kidney disease.

At the end of 2007, more than 3000 people in New Zealand and 17,578 people in Australia were receiving KRT. More than 10,000 of these Australians were receiving regular dialysis and the rest were living with a functioning kidney transplant.²² Of those on dialysis, 69% were receiving HD in a hospital or satellite centre attached to a hospital, and the remainder were receiving dialysis at home.

The Australian and New Zealand Indigenous populations are disproportionately affected by CKD, particularly ESKD.²¹ Indigenous Australians account for approximately 9% of all ESKD patients and Māori account for 31% of ESKD patients in New Zealand. The incidence of ESKD in Indigenous Australians is 8–30 times the national average depending on which state/territory the person is located in; the higher rates reflect rural and remote locations.^21,²² In the Northern Territory, for example, the rate is doubling every 3–4 years. Indigenous people are also less likely to be living with a functioning transplant compared to their non-Indigenous counterparts, meaning a far greater proportion are reliant on dialysis for KRT.^21,²⁴ A number of factors contribute to this, including the generally poorer socioeconomic situation of Indigenous populations, their higher rates of risk factors, the time to diagnosis and access to treatment centres. Difficulties with spoken and written English, lack of available transport, financial difficulties and the proximity of culturally appropriate healthcare services all present barriers to Indigenous people accessing healthcare.²⁴ Approximately 50% of Indigenous Australians are required to relocate to urban or regional areas in order to receive KRT. This has a significant impact and burden on the emotional, social, physical and financial wellbeing of individuals.

Every patient with ESKD, regardless of age, should be offered dialysis unless it is medically contraindicated or the patient refuses treatment. In New Zealand and Australia, government-sponsored healthcare (e.g. Medicare) covers the cost of dialysis and transplant treatment. Some private health insurance companies will also reimburse some of the costs associated with ESKD treatment. However, for many patients, especially those living in rural or remote areas, ready access to treatment is a major difficulty.

In Australia, Kidney Health Australia is actively supporting strategies to prevent and reduce the risk of CKD. Guidelines for clinical practice have also been developed under the auspices of Caring for Australasians with Renal Impairment (CARI), which assists nurses in both New Zealand and Australia.²⁵ In addition, the National Kidney Foundation (United States) Kidney Disease Outcomes Quality Initiative (K/DOQI) has contributed to nursing practice in New Zealand and Australia with its clinical guidelines to manage patients in the early stages of kidney disease by slowing disease progression, detecting/treating complications and managing cardiovascular risk factors.

CLINICAL MANIFESTATIONS

As renal function progressively deteriorates, every body system becomes affected. The clinical manifestations are a result of retained substances, including urea, creatinine, phenols, hormones, electrolytes, water and many other substances. Uraemia is a syndrome that incorporates all the signs and symptoms seen in the various systems throughout the body in CKD (see Fig 46-5). It is important to recognise that the manifestations of uraemia vary among patients according to the cause of the kidney disease, coexisting conditions, and the patient’s age and degree of compliance with the prescribed medical regimen. Many patients are very tolerant of the changes that occur because they develop gradually.

Figure 46-5 Clinical manifestations of chronic uraemia.

Urinary system

In the early stage of renal insufficiency, polyuria results from the inability of the kidneys to concentrate urine. This happens most often at night and the patient must rise several times to urinate (nocturia). Because of the decrease in renal concentrating ability, the specific gravity of urine gradually becomes fixed at about 1.010 (the osmolar concentration of plasma). Since diabetes is the primary cause of CKD, polyuria may be present, but not necessarily as a consequence of kidney disease. Because most people continue to have good urine output, it is often difficult to convince patients that they have kidney disease. As CKD progresses, patients will have increasing difficulty with fluid retention and require diuretic therapy, and often oliguria develops. Proteinuria, casts, pyuria and haematuria could be present depending on the cause of the kidney disease. Once on dialysis and/or after a period of time on dialysis, patients may develop anuria (urine output <100 mL per 24 hours).

Metabolic disturbances

Waste product accumulation

As the GFR decreases, the serum urea and creatinine levels increase. The urea is increased not only by the kidney failure but also by protein intake, fever, corticosteroids and catabolism. For this reason, serum creatinine and creatinine clearance determinations are considered more accurate indicators of kidney function than serum urea levels.¹⁹ As serum urea levels increase, nausea, vomiting, lethargy, fatigue, impaired thought processes and headaches become common as a result of the presence of waste products in the central nervous system (CNS) and GI system.

The serum creatinine level in an older patient with ESKD will be lower than in a younger person with the same degree of renal dysfunction.²⁶ Decreased muscle mass and decreased muscle activity from ageing account for this finding because creatinine is an end product of muscle metabolism.

Altered carbohydrate metabolism

Defective carbohydrate metabolism is caused by impaired glucose use resulting from cellular insensitivity to the normal action of insulin. The exact nature of this insulin resistance is unclear but it may be related to circulating insulin antagonists, alterations in hormone receptors or abnormalities of transport mechanisms. Moderate hyperglycaemia, hyperinsulinaemia and abnormal glucose tolerance tests may be seen. Insulin and glucose metabolism may improve (but not to normal values) after the initiation of dialysis.

Patients with diabetes who become uraemic may require less insulin than before the onset of CKD. This is because insulin, which is dependent on the kidneys for excretion, remains in the circulation longer. The insulin dosing must be individualised and glucose levels monitored carefully.²⁷

Elevated triglycerides

Hyperinsulinaemia stimulates hepatic production of triglycerides. Almost all patients with CKD develop hyperlipidaemia, with elevated very-low-density lipoproteins (VLDLs), normal or decreased low-density lipoproteins (LDLs) and decreased high-density lipoproteins (HDLs). The altered lipid metabolism is related to decreased levels of the enzyme lipoprotein lipase, which is important in the breakdown of lipoproteins. Hyperlipidaemia is a risk factor for accelerated atherosclerosis (see Ch 37) and it can worsen atherosclerotic changes in diabetics with ESKD.²⁸

The serum level of triglycerides does not usually decrease after dialysis is started. For patients receiving long-term PD, the level frequently becomes higher as a result of the increased amounts of glucose absorbed from the peritoneal dialysate fluid. Elevated glucose levels lead to increased insulin levels. Insulin stimulates the liver to produce triglycerides.

Electrolyte and acid–base imbalances

Potassium

Hyperkalaemia (raised serum potassium) is the most serious electrolyte disorder associated with kidney disease. Fatal arrhythmias can occur when the serum potassium level reaches 7–8 mmol/L. Hyperkalaemia results from the decreased excretion by the kidneys, the breakdown of cellular protein, bleeding and metabolic acidosis. Potassium may also come from the food consumed, dietary supplements, medications and IV infusions.²⁸

Sodium

Sodium levels may be normal or low in CKD. Because of impaired sodium excretion, sodium is retained along with water. If large quantities of body water are retained, dilutional hyponatraemia occurs. Sodium retention can contribute to oedema, hypertension and heart failure. Sodium intake must be individually determined but is generally restricted to 2 g/day.

Calcium and phosphate

The kidneys play a pivotal role in the management of calcium and phosphate along with the activation of vitamin D, which is significantly disrupted in CKD. In patients with CKD stages 3 and 4, it is evident that there are abnormalities in bones and almost no patient on dialysis has normal bone histology.²⁸ CKD mineral and bone disorder (CKD–MBD) is a broad clinical disorder that has a profound impact on morbidity and mortality.²⁹ Calcium and phosphate alterations are discussed in the section on the musculoskeletal system below.

Magnesium

Magnesium is primarily excreted by the kidneys. Hypermagnesaemia is generally not a problem unless the patient is ingesting magnesium (e.g. milk of magnesia, magnesium citrate, antacids containing magnesium). Clinical manifestations of hypermagnesaemia can include absence of reflexes, decreased mental status, cardiac arrhythmias, hypotension and respiratory failure.

Metabolic acidosis

Metabolic acidosis results from the impaired ability of the kidneys to excrete the acid load (primarily ammonia) and from defective reabsorption and regeneration of bicarbonate. The average adult produces 80–90 mmol of acid per day. This acid is normally buffered by bicarbonate. In CKD, the plasma bicarbonate level, which is an indirect measure of acidosis, usually falls to a new steady state of 16–20 mmol/L. The decrease in plasma bicarbonate reflects its use in buffering metabolic acids. It generally does not fall below this level because hydrogen ion production is usually balanced by buffering from demineralisation of the bone (phosphate buffering system). Although Kussmaul respirations are uncommon in CKD, this breathing pattern reduces the severity of acidosis by increasing carbon dioxide excretion.

Haematological system

Anaemia

A normocytic or normochromic anaemia is associated with CKD. The anaemia is due to decreased production of the hormone erythropoietin by the kidneys, which is caused by the decrease in functioning renal tubular cells.²⁸ Erythropoietin normally stimulates precursor cells in the bone marrow to produce RBCs (erythropoiesis). Other factors contributing to anaemia are nutritional deficiencies, decreased RBC life span, increased haemolysis of RBCs, frequent blood samplings and bleeding from the GI tract. For patients receiving maintenance HD, blood loss in the dialyser may also contribute to the anaemic state. Elevated levels of PTH (produced to compensate for low serum calcium levels) can inhibit erythropoiesis, shorten the survival of RBCs and cause bone marrow fibrosis, which can result in decreased numbers of haematopoietic cells.

Sufficient iron stores are needed for erythropoiesis. Many patients with CKD are iron deficient and require iron replacement. Folic acid, which is essential for RBC maturation, is dialysable. If it is not adequately replaced in the diet or by supplements, megaloblastic anaemia may develop in the patient receiving chronic HD.

Bleeding tendencies

The most common cause of bleeding in uraemia is a qualitative defect in platelet function. This dysfunction is caused by impaired platelet aggregation and impaired release of platelet factor 3. In addition, alterations in the coagulation system with increased concentrations of both factor VIII and fibrinogen are found in the serum of these patients. The altered platelet function, haemorrhagic tendencies and GI bleeding can usually be corrected with regular HD or PD.

Infection

Patients with advanced CKD have an increased susceptibility to infection. Infectious complications are caused by changes in leucocyte function and altered immune response and function. There is a diminished inflammatory response because of an altered chemotactic response by both neutrophils and monocytes. This impairment significantly decreases the accumulation of WBCs at the site of injury or infection. Characteristic clinical findings include lymphopenia, lymphoid tissue atrophy (especially of the thymus), decreased antibody production and suppression of the delayed hypersensitivity response. Other factors contributing to the increased risk of infection include malnutrition, hyperglycaemia and external trauma (e.g. catheters, needle insertions into vascular access sites).

Increased incidence of cancer

There is a significant increase in the incidence of neoplasms in the patient with CKD compared to the general population. Lung, breast, uterus, colon, prostate and skin malignancies are most commonly found.³⁰

Cardiovascular system

Traditional cardiovascular risk factors such as hypertension and elevated lipids are common in CKD patients. However, much of the cardiovascular disease may be related to non-traditional cardiovascular risk factors such as vascular calcification and arterial stiffness, which are major contributors to cardiovascular disease in CKD. The calcium deposits in the vascular medial layer are associated with stiffening of the blood vessels. The mechanisms involved are multifactorial and incompletely understood. They include: (1) vascular smooth muscle cells changing into chondrocyte or osteoblast-like cells; (2) high total body amount of calcium and phosphate due to abnormal bone metabolism; (3) impaired renal excretion; and (4) drug therapies to treat the bone disease (e.g. calcium phosphate binders).

Cardiovascular disease is the most common cause of death in patients with CKD. Even a slight reduction in the GFR has been associated with a higher risk for the development of coronary artery disease. Cardiovascular disease and CKD are so closely linked that patients who develop cardiac events (e.g. myocardial infarction, heart failure) are recommended to have an evaluation of their kidney function.

Hypertension is highly prevalent in patients with CKD because hypertension is both a cause and a consequence of CKD. Hypertension is aggravated by sodium retention and increased extracellular fluid volume.²⁸ In some individuals, increased renin production contributes to hypertension (see Fig 44-4).

Hypertension and diabetes mellitus are contributing risk factors for the development of vascular complications. The vascular changes that result from longstanding hypertension and the accelerated atherosclerosis due to elevated triglyceride levels are responsible for many cardiovascular complications (e.g. myocardial infarction). Myocardial infarction, ischaemic heart disease, peripheral arterial disease, heart failure, cardiomyopathy and stroke are leading causes of death for patients receiving long-term dialysis. Left ventricular hypertrophy resulting from longstanding hypertension, extracellular fluid volume overload and anaemia leads to cardiomyopathy and heart failure.³¹ Pulmonary oedema and peripheral oedema can occur.

Cardiac arrhythmias may result from hyperkalaemia, hypocalcaemia and decreased coronary artery perfusion. Uraemic pericarditis can develop and occasionally progresses to pericardial effusion and cardiac tamponade. Pericarditis is manifested by a friction rub, chest pain and low-grade fever.

In addition to direct cardiovascular effects, hypertension can cause retinopathy, encephalopathy and nephropathy. Because of the many effects, blood pressure control is one of the most important therapeutic goals in the management of CKD.²⁸

Respiratory system

Respiratory changes include Kussmaul respirations (to compensate for metabolic acidosis), dyspnoea from fluid overload, pulmonary oedema, uraemic pleuritis (pleurisy), pleural effusion and a predisposition to respiratory infections, which may be related to decreased pulmonary macrophage activity. The sputum is thick and tenacious. The cough reflex is depressed. ‘Uraemic lung’, or uraemic pneumonitis, is typically found in people with CKD and shows up as interstitial oedema on chest X-ray. This condition usually responds to vigorous fluid removal during dialysis treatment.

Gastrointestinal system

Every part of the GI system is affected as a result of inflammation of the mucosa caused by excessive urea. Mucosal ulcerations, found throughout the GI tract, are caused by the increased ammonia produced by bacterial breakdown of urea. Stomatitis with exudates and ulcerations, a metallic taste in the mouth and uraemic fetor (a urinous odour of the breath) are commonly found.²⁸ Anorexia, nausea and vomiting caused by irritation of the GI tract by waste products contribute to weight loss and malnutrition. Diabetic gastroparesis can compound these problems for patients with diabetes. GI bleeding is also a risk because of irritation to the mucosa by waste products, coupled with the platelet defect. Diarrhoea may occur because of hyperkalaemia and altered calcium metabolism. Constipation may be due to the ingestion of iron salts and/or calcium-containing phosphate binders (e.g. calcium carbonate). Constipation can be made worse by the limited fluid intake and inactivity.

Neurological system

Neurological changes are expected as CKD progresses. They are attributed to increased nitrogenous waste products, electrolyte imbalances, metabolic acidosis, and axonal atrophy and demyelination of nerve fibres.³² High levels of waste toxins have been implicated in axonal damage.

In CKD a general depression of the CNS results in lethargy, apathy, decreased ability to concentrate, fatigue, irritability and altered mental ability. Seizures and coma may result from a rapidly increasing serum urea level and hypertensive encephalopathy. Dialysis encephalopathy (dialysis dementia), a progressive neurological impairment associated with aluminium toxicity, is characterised by speech disturbances, dementia, lack of muscle coordination and myoclonic seizures. Aluminium toxicity is now uncommon because aluminium-based drugs have been replaced.

Peripheral neuropathy is initially manifested by a slowing of nerve conduction to the extremities. The patient complains of restless legs syndrome (described in Ch 58) and may describe it as ‘bugs crawling inside the leg’. Paraesthesias are most often experienced in the feet and legs and may be described by the patient as a burning sensation. Eventually, motor involvement may lead to bilateral foot drop, muscular weakness and atrophy, and loss of deep tendon reflexes. Muscle twitching, jerking, asterixis (hand-flapping tremor) and nocturnal leg cramps also occur. In patients with diabetes, uraemic neuropathy is compounded by the neuropathy associated with diabetes mellitus.

The treatment for neurological problems is dialysis or transplantation. Altered mental status is often the signal that dialysis must be initiated. Dialysis should improve the general CNS symptoms and may slow or halt the progression of neuropathies. However, motor neuropathy may not be reversible.

Musculoskeletal system

CKD-MBD has replaced the traditional concept of renal osteodystrophy and explains the different skeletal changes found in CKD that result from alterations in calcium and phosphate metabolism (see Fig 46-6).^28,²⁹ Normally the calcium/phosphate ratio maintains the electrolytes in a soluble state. When calcium levels decline, the parathyroid glands release PTH. PTH stimulates the kidneys to activate vitamin D, which promotes absorption of calcium from the bowel. PTH also increases calcium resorption by the kidneys, phosphate excretion by the kidneys and release of calcium from the bone. Calcium and phosphate levels return to normal and secretion of PTH is reversed.

Figure 46-6 Mechanisms of CKD mineral and bone disorder (CKD-MBD). GFR, Glomerular filtration rate; PO₄, phosphate; PTH, parathyroid hormone.

However, in CKD, as the GFR decreases, urinary phosphate excretion is impaired and the serum phosphate levels increase. The kidneys fail to activate vitamin D, calcium absorption is impaired and serum calcium decreases. Low serum calcium and high serum phosphate levels stimulate the release of PTH, which causes resorption of calcium and phosphate from the bone. This release increases serum calcium as well as serum phosphate levels. The excess phosphate binds with calcium, leading to the formation of insoluble metastatic calcifications that are deposited throughout the body. Common sites are the muscles, lungs, skin and subcutaneous tissue, GI tract, walls of blood vessels and the eyes.³² ‘Uraemic red eye’ is caused by irritation from deposits in the eye. CKD-MBD can lead to non-specific symptoms such as pain and stiffness in the joints, predisposition to fracture and muscle weakness. It can also cause cardiovascular calcification and calciphylaxis.³³ In addition, there is a strong association with accelerated risk of stroke, amputation, disruption of the conduction system and cardiac arrest. The complication of CKD-MBD contributes significantly to the patient’s increased morbidity and mortality risks.

There are three components to CKD-MBD:

• Bone turnover describes the skeletal remodelling process that occurs as old bone is replaced with healthy new bone (the balance between bone resorption and formation). It can be classified as low, normal or high.

• Bone mineralisation describes the efficiency of collagen calcification during the formation phase of skeletal remodelling and can be classified as either normal or abnormal.

• Bone volume is an indication of the amount of bone per unit volume and is classified as normal, low or high.³³

The abnormalities in CKD-MBD are described in terms of the interactions among these three components and result in four types of renal osteodystrophy: (1) osteomalacia; (2) adynamic bone disease; (3) osteitis fibrosa; and (4) mixed uraemic osteodystrophy.³³

Integumentary system

The skin appears pale as a result of anaemia and is dry and scaly because of a decrease in oil and sweat gland activity. Decreased perspiration results from a decrease in the size of the sweat glands. People in CKD stages 4 or 5 may also have a yellow–grey discolouration of the skin. This change is a result of the absorption and retention of urinary pigments that normally give the characteristic colour to urine.²⁸

Pruritus most commonly results from a combination of dry skin, calcium phosphate deposition in the skin and sensory neuropathy. The itching may be so intense that it can lead to bleeding or infection secondary to scratching. Uraemic frost is a rare condition in which urea crystallises on the skin; it is usually seen only when serum urea levels are extremely high. It occurs when a patient refuses dialysis or is withdrawn from dialysis.

The hair is dry and brittle and may fall out. The nails are thin, brittle and ridged. Petechiae and ecchymoses may be present and are due to platelet abnormalities.²⁸

Reproductive system

Both sexes characteristically experience infertility and a decreased libido with CKD. Women usually have decreased levels of oestrogen, progesterone and luteinising hormone, causing anovulation and menstrual changes (usually amenorrhoea). Menses and ovulation may return after dialysis is started. Men experience loss of testicular consistency, decreased testosterone levels and low sperm counts. Sexual dysfunction in both sexes may also be caused by anaemia, which causes fatigue and decreased libido. In addition, peripheral neuropathy can cause impotence in men and anorgasmy in women. Additional factors that may cause changes in sexual function are psychological problems (e.g. anxiety, depression), physical stress and the side effects of drugs.

Sexual function may improve with maintenance dialysis and may become normal with successful transplantation. Pregnant dialysis patients have been able to carry a fetus to term, but there is significant risk to the mother and infant. Pregnancy in transplant patients is more common, but there is also a risk to both the mother and the fetus.

Endocrine system

Many patients with CKD exhibit some clinical manifestations of hypothyroidism. Tests of thyroid function may yield low to low–normal levels for serum triiodothyronine (T₃) and thyroxine (T₄). Neither the clinical significance nor the exact cause of these findings is known.

Psychological changes

Numerous psychological changes are experienced by patients with CKD.³⁴ Personality and behavioural changes, emotional lability, withdrawal and depression are commonly observed. However, it is important that these symptoms are not simply assumed to be part of CKD and that patients who have treatable depression are treated. Fatigue and lethargy contribute to the feeling of illness. The changes in body image caused by oedema, integumentary disturbances and access devices (e.g. fistulas, catheters) lead to further anxiety and depression. Decreased ability to concentrate and slowed mental activity can give the appearance of dullness and disinterest in the environment. There are also significant changes in lifestyle, occupation, family responsibilities and financial status that the patient must deal with. Long-term survival depends on medications, dietary restrictions, dialysis and possibly transplantation. The patient will also grieve the loss of kidney function. This can be a prolonged process for some individuals.

DIAGNOSTIC STUDIES

Adverse outcomes of CKD can often be prevented or delayed through early detection and treatment. Because persistent proteinuria is usually the first indication of kidney damage, screening for CKD involves a dipstick evaluation of protein in the urine. A person with persistent proteinuria (1+ protein on standard dipstick testing two or more times over a 3-month period) should have further assessment of risk factors and a diagnostic examination with blood and urine tests. A urine test for the albumin-to-creatinine ratio (ACR) or protein-to-creatinine ratio (PCR) provides an accurate estimate of the albumin or protein excretion rate. Current CKD guidelines may recommend either an ACR test or a PCR test be performed, although recent evidence suggests that the ACR might be better for patients with diabetes and the PCR for non-diabetic patients.³⁵ A ratio greater than 300 mg of albumin per 1 g of creatinine signals CKD.

Many consider serum creatinine as the best indicator of kidney function, but in reality serum creatinine alone poorly reflects kidney function. The GFR is the preferred measure used to determine kidney function. Several GFR calculators are available. Kidney Health Australia recommends the Modification of Diet in Renal Disease (MDRD) Study equation to estimate the GFR (see Table 46-7).

TABLE 46-7 Serum creatinine alone is poor indicator of kidney function

GFR, glomerular filtration rate; MDRD, modification of diet in renal disease.

† GFR as estimated by the MDRD equation calculator can be accessed at www.kidney.org.au/HealthProfessionals/eGFRClinicalTools/tabid/632/Default.aspx.

A urinalysis can detect RBCs, WBCs, protein, casts and glucose. Imaging of the kidneys to exclude obstruction and note the size of the kidneys is usually achieved by ultrasound. Other diagnostic studies, as noted in Box 46-3, help establish the diagnosis and cause of CKD.

MULTIDISCIPLINARY CARE

When a patient is diagnosed as having CKD, conservative therapy is attempted before maintenance dialysis begins (see Box 46-3). Every effort is made to detect and treat potentially reversible causes of CKD (e.g. cardiac failure, dehydration, infections, nephrotoxins, urinary tract obstruction, glomerulonephritis, renal artery stenosis). A renal biopsy may be necessary to provide a definitive diagnosis. The goals of conservative therapy are to preserve existing kidney function, treat the clinical manifestations, prevent complications and provide for the patient’s comfort. Through early recognition, diagnosis and appropriate treatment, it has been shown that the progression of CKD can be slowed, quality of life can be maintained and outcomes for these individuals can be improved.³⁶ A focus on stages 1–4 (see Table 46-6) prior to the need for dialysis (stage 5) includes the control of hyperkalaemia, hypertension, hyperparathyroid disease, anaemia, hyperglycaemia and dyslipidaemia.²⁸ If hypothyroidism is present, it is also treated. Laboratory analysis, drug and nutritional therapy and supportive care are essential components of the conservative treatment plan. The following section focuses primarily on the drug and nutritional aspects of care.

Most patients with ESKD are treated with dialysis rather than transplantation because: (1) there is a lack of donated organs; (2) some patients are physically or mentally unsuitable for transplantation; or (3) some patients do not want transplants. With advances in medical science, an increasing number of individuals are receiving maintenance dialysis, including the elderly and those with complex medical problems. A patient’s chronological age is not a factor in determining candidacy for dialysis. Factors that are important are the patient’s ability to cope and the existing support system.

Drug therapy

Hyperkalaemia

There are multiple strategies for managing hyperkalaemia (see Box 46-2). Every effort is made to control hyperkalaemia with the restriction of high-potassium foods and drugs.²⁸ Acute hyperkalaemia may require treatment with IV glucose and insulin or IV 10% calcium gluconate. Sodium (or calcium) polystyrene sulfonate, a cation-exchange resin, is commonly used to lower potassium levels in CKD stage 4 and can be administered on an outpatient basis. The patient should be told to expect some constipation, and it is often advisable to concurrently administer a laxative such as lactulose to ensure evacuation of the potassium from the bowel. It should never be given to a patient with a hypoactive bowel (paralytic ileus) because fluid shifts could lead to bowel necrosis. As sodium polystyrene sulfonate exchanges sodium ions for potassium ions, the patient should be observed for sodium and water retention.²⁸ If life-threatening arrhythmias are present, dialysis may be required to remove excess potassium.

Hypertension

The progression of CKD can be delayed by controlling hypertension. (Control and treatment of hypertension are discussed in Ch 32.) It is recommended that the target blood pressure be less than 130/80 mmHg for patients with CKD or diabetes.³⁷ Treatment of hypertension includes: (1) weight loss (if obese); (2) therapeutic lifestyle changes (i.e. exercise, avoidance of alcohol, smoking cessation); (3) diet recommendations (DASH diet; see Ch 33); and (4) administration of antihypertensive drugs.

The antihypertensive drugs most commonly used are diuretics (e.g. furosemide), β-adrenergic blockers (e.g. atenolol), ACE inhibitors (e.g. ramipril), angiotensin receptor blocker (ARB) agents (e.g. losartan) and calcium channel blockers (e.g. amylodipine). Prescribed medications are dependent on whether the patient is diabetic or non-diabetic. Diuretics and β-adrenergic blockers are the recommended initial therapy for non-diabetics. ACE inhibitors and ARBs are used for diabetics and those with non-diabetic proteinuria because they decrease proteinuria and delay the progression of CKD.^26,³⁷ However, they must be used cautiously when ESKD occurs because they can further decrease the GFR and increase serum potassium levels. Patients with CKD are likely to require more than two different agents to control blood pressure.³³

The patient’s blood pressure should be measured periodically in supine, sitting and standing positions to monitor the effect of antihypertensive drugs. Patients and their families should be taught how to monitor their blood pressure at home and what readings require immediate intervention. Blood pressure control is essential to slow atherosclerotic changes that could further impair kidney function.

CKD-mineral and bone disorder

The CARI clinical practice guidelines provide information to assist in the care of patients with CKD-MBD.³⁸ Interventions include limiting dietary phosphorus, administering phosphate binders, supplementing vitamin D and controlling hyperparathyroidism.²¹

Phosphate intake is generally restricted to less than 1000 mg per day, but dietary control alone is usually inadequate. Calcium-based phosphate binders such as calcium carbonate and calcium acetate are used to bind phosphate in the bowel, which is then excreted in the stool. Giving a calcium-based binder when serum phosphate levels are still high (>1.98 mmol/L) may cause the formation of systemic calcium phosphate deposits. Sevelamer is a new phosphate binder that does not contain either calcium or aluminium, and it has the added benefits of lowering cholesterol and LDLs.³⁸ The newest drug to reduce serum phosphorus levels, lanthanum carbonate, also does not contain either calcium or aluminium, and it has the added benefit that it is a chewable tablet.^32,³⁸ Phosphate binders must be administered with each meal to be effective, because most phosphate is absorbed within 1 hour after eating. Constipation is a frequent side effect of phosphate binders and may necessitate the use of stool softeners.

Because dementia (aluminium toxicity) and bone disease (osteomalacia) are associated with excessive absorption of aluminium, aluminium preparations such as AluTab should be used with caution in patients with renal insufficiency. Magnesium-containing antacids (Mylanta) should not be used, because magnesium is dependent on the kidneys for excretion.

Hypocalcaemia is often a problem because of the GI tract’s inability to absorb calcium in the absence of vitamin D. If hypocalcaemia persists in the setting of controlled serum phosphate levels and supplemental calcium, the active form of vitamin D should be given.³⁹ Vitamin D levels need to be assessed. If the levels are low (serum values less than 30 ng/mL), vitamin D supplementation in the form of cholecalciferol is recommended.

Treatment of secondary hyperparathyroidism also requires the activated form of vitamin D, because the kidneys no longer possess the ability to activate vitamin D. Active vitamin D is available as oral or IV calcitriol. It is important that the serum phosphate level is lowered before administering calcium or vitamin D because these drugs may contribute to soft-tissue calcification. Hypercalcaemia may occur with calcium and vitamin D supplementation and is associated with increased cardiac calcifications and mortality in ESKD patients. If hypercalcaemia occurs, dosages of vitamin D and calcium-based phosphate binders should be reduced and dietary calcium restricted. Non-calcium-based phosphate binders could also be substituted.³⁸

Calcimimetic agents are a new class of drugs used to control secondary hyperparathyroidism. Cinacalcet increases the sensitivity of the calcium receptors in the parathyroid glands. As a result, the parathyroid glands detect calcium at lower serum levels and decrease PTH secretion. Cinacalcet is currently used only for patients on dialysis, but its role in the treatment of CKD-MBD at earlier stages is under investigation.^38,³⁹

If CKD-MBD remains severe despite conservative therapy, a subtotal parathyroidectomy may be performed to decrease the synthesis and secretion of PTH. In some situations a total parathyroidectomy is performed and some parathyroid tissue is transplanted into the forearm. The transplanted cells produce PTH as needed. If production of PTH becomes excessive, some of the cells can be removed from the forearm using local anaesthesia.

The most common methods for evaluating the status of bone disease are skeletal X-rays, bone scans, bone biopsy and bone densitometry.³⁸ PTH and alkaline phosphatase levels should also be measured. Alkaline phosphatase is elevated when there is demineralisation of the bone but can be increased by liver disease.

Anaemia

The most important cause of anaemia is a decreased production of erythropoietin due to the decrease in the number of functioning renal tubular cells.⁴⁰ Anaemia in CKD patients also causes congestive heart failure and the high incidence of cardiovascular deaths.⁴¹ CARI guidelines recommend that haemoglobin levels should be 110 –120 g/L and haematocrit should be about 39% for patients with CKD.⁴² With the use of recombinant deoxyribonucleic acid (DNA) technology (see Ch 13), erythropoietin-stimulating agent can be produced and is available for the treatment of anaemia (e.g. epoetin alfa, epoetin beta, darbepoetin alfa). It can be administered intravenously or subcutaneously and has proven to be very effective. A significant increase in haemoglobin and haematocrit levels is usually not seen for 2–3 weeks. The patient who is receiving erythropoietin-stimulating agent has improved cardiac performance and exercise tolerance and an enhanced quality of life.

A common adverse effect of exogenous erythropoietin is the development or acceleration of hypertension. The underlying mechanism is related to the haemodynamic changes (e.g. increased whole blood viscosity) that occur as the anaemia is corrected. Another side effect is the development of functional iron deficiency resulting from the increased demand for iron to support erythropoiesis. Intravenous iron supplements are recommended if the plasma ferritin concentrations fall below 100 ng/mL.⁴³ Supplemental folic acid (1 mg daily) is usually given because it is needed for RBC formation and is removed by dialysis.

Blood transfusions should be avoided in treating anaemia unless the patient experiences an acute blood loss or has symptomatic anaemia (i.e. dyspnoea, excess fatigue, tachycardia, palpitations, chest pain). Undesirable effects of transfusions are the suppression of erythropoiesis as a result of a decrease in the hypoxic stimulus and the possibility of iron overload because each unit of blood contains about 250 mg of iron.

Dyslipidaemia

A common problem of progressive CKD is that of dyslipidaemia, a primary risk factor for cardiovascular disease and early death. Recommendations for patients with CKD include a goal of lowering LDLs below 2.6 mmol/L and maintaining a triglyceride level below 2.25 mmol/L.⁴⁴ Statins (HMG-CoA reductase inhibitors) are the most effective drugs for lowering LDL cholesterol levels. Fibrates (fibric acid derivatives) are the most effective drugs available for lowering triglyceride levels and can also increase HDL levels.⁴⁴ Specific drugs of these classes that are used depend on the individual patient response and the recommendations of the treating doctor.

Complications of drug therapy

Many drugs are partially or totally excreted by the kidneys. Delayed and decreased elimination lead to an accumulation of drugs and the potential for drug toxicity. Drug doses and frequency of administration must be adjusted based on the severity of the kidney disease.⁴⁵ Increased sensitivity may result as drug levels increase in the blood and tissues. Drugs of particular concern include digoxin, diabetic agents (metformin), antibiotics (e.g. vancomycin, gentamicin) and opioid medications.

Digoxin is excreted largely by the kidneys. While loading doses may not need to be changed, maintenance doses and frequency of digoxin may have to be adjusted. Many patients require only 125 μg every other day. Dialysis does not affect body levels of digoxin but it does affect potassium levels. Hypokalaemia can potentiate the action of digoxin.

Aminoglycosides, penicillin in high doses and tetracyclines are potentially nephrotoxic and require dose and frequency adjustments. The frequency and dose of vancomycin and gentamicin must be decreased because they are dependent on the kidneys for excretion. These drugs can accumulate to toxic levels if appropriate adjustments are not made.

Pethidine should never be administered to a patient with CKD because the liver metabolises it to norpethidine, which is dependent on the kidneys for excretion. If norpethidine accumulates, seizures can result. Other pain medications may be given but less frequently and in smaller doses (e.g. paracetamol, oxycodone, morphine sulphate).

Patients should be advised to avoid NSAIDs. These drugs block the synthesis of the renal prostaglandins that promote vasodilation. This can worsen renal hypoperfusion. Many NSAIDs are available over-the-counter, so it is essential that the patient be cautioned. Paracetamol can be substituted.

Nutritional therapy

Protein restriction

The diet is designed to be as normal as possible to maintain good nutrition (see Table 46-8). Kilojoule-protein malnutrition is a potential and serious problem that results from altered metabolism, anaemia, proteinuria, anorexia and nausea.⁴⁶ Additional factors leading to malnutrition include depression and complex diets that restrict protein, phosphorus, potassium and sodium. Frequent monitoring of laboratory parameters, especially serum albumin and ferritin, and anthropometric measurements are necessary to evaluate nutritional status. All patients with CKD should be referred to a dietician for nutritional education and guidance.

TABLE 46-8 Daily recommendations for the patient with chronic kidney disease ^*

NUTRITIONAL THERAPY

EDW, estimated dry weight; IBW, ideal body weight.

* Diets must be individualised in accordance with needs.

For the patient who is undergoing dialysis, protein is not routinely restricted (see Table 46-8). The beneficial role of protein restriction in CKD stages 1–4 as a means to reduce the decline in kidney function is currently being studied (see the Evidence-based practice box). Historically, dietary counselling often encouraged a restriction in protein for individuals with CKD. Although there is some evidence that protein restriction has benefits, many patients find these diets difficult to adhere to. For CKD stages 1–4, many clinicians just encourage a diet with normal protein intake. However, it advisable to teach patients to avoid high-protein diets and supplements, as they may overstress the diseased kidneys.

Does a low-protein diet delay onset of chronic kidney disease?

EVIDENCE-BASED PRACTICE

Clinical question

For non-diabetic patients with chronic kidney disease (CKD) (P), does maintaining a low-protein diet (I) versus usual protein intake (C) delay the onset of end-stage kidney disease (O)?

Best available evidence

• Systematic review of randomised controlled trials (RCTs)

Conclusion

• Diets that restrict protein to 0.6 g/kg/day can delay end-stage kidney disease in non-diabetic adults with CKD.

Reference for evidence

Fouque D, Laville M. Low protein diets for chronic kidney disease in non diabetic adults. Cochrane Database Syst Rev. (3):2009. CD001892.

Dietary protein guidelines for PD differ from those for HD because of protein loss in the dialysate. During PD, protein intake must be high enough to compensate for the losses so that the nitrogen balance is maintained. The recommended protein intake is at least 1.2 g/kg of ideal body weight per day and can be increased depending on the individual needs of the patient.²⁸

For patients with malnutrition or inadequate energy or protein intake, commercially prepared products that are high in protein but low in sodium and potassium are available (e.g. Nepro, Amin-Aid). As an alternative, liquid or powder breakfast drinks may be purchased from supermarkets.

Water restriction

Water intake depends on the daily urine output. Patients on HD have a more restricted diet than patients receiving PD. For those receiving HD, as their urinary output diminishes, fluid restrictions are enhanced. Intake depends on the daily urine output. Generally, 600 mL (from insensible loss) plus an amount equal to the previous day’s urine output is allowed for a patient with CKD who is not receiving HD. Foods that are liquid at room temperature (e.g. gelatine, ice-cream) should be counted as fluid intake. The fluid allocation should be spaced throughout the day so that the patient does not become thirsty. For the patient on long-term HD, fluid intake is adjusted so that weight gains are no more than 1–3 kg between dialyses.

Sodium and potassium restriction

Sodium and potassium restriction depends on the ability of the kidneys to excrete these electrolytes. Sodium-restricted diets may vary from 2 g to 4 g depending on the degree of oedema and hypertension. Sodium and salt should not be equated because the sodium content in 1 g of sodium chloride is equivalent to 400 mg of sodium. The patient should be instructed to avoid high-sodium foods such as cured meats, pickled foods, canned soups and stews, soy sauce, salad dressings and Vegemite. Most salt substitutes should not be used because they contain potassium chloride.

Dietary restrictions for potassium range from about 2 g to 4 g (39 mg = 1 mmol). Some patients on PD do not need potassium restrictions. Foods with high potassium content that should be avoided include oranges, bananas, melons, tomatoes, prunes, raisins, deep-green and yellow vegetables, beans and legumes (see Table 46-9).

TABLE 46-9 High-potassium foods

NUTRITIONAL THERAPY

Phosphate restriction

Phosphate should be limited to approximately 1000 mg a day. Foods that are high in phosphate include dairy products (e.g. milk, ice-cream, cheese, yoghurt) and foods containing dairy products (e.g. puddings). Most foods that are high in phosphate are also high in calcium. Restricting phosphate will restrict calcium intake.

NURSING MANAGEMENT: CONSERVATIVE THERAPY OF CHRONIC KIDNEY DISEASE

Nursing assessment

The nurse should obtain a complete history of any existing kidney disease or a family history of kidney disease because some kidney disorders have a hereditary basis, including Alport’s syndrome and polycystic kidney disease. Other disorders that can lead to CKD are diabetes mellitus, hypertension and systemic lupus erythematosus. Because many drugs are potentially nephrotoxic, the patient should be asked about both current and past use of prescription and over-the-counter drugs and herbal preparations.

Antacids that contain magnesium and aluminium should be avoided since patients with kidney disease are no longer able to rid the body of these substances. Some antacids contain high levels of salt, contributing to worsening hypertension. In addition, antacids may interfere with absorption of other medications.

NSAIDs (aspirin, ibuprofen, naproxen) can contribute to the development of AKI and the progression of CKD, especially when taken in higher doses than recommended. Analgesics in combination and in large quantities have been associated with the development of kidney failure. If taken as prescribed for short periods of time, these analgesics are usually considered safe.

Decongestants and antihistamines that contain pseudoephedrine may contribute to worsening of hypertension. Phenylephrine and pseudoephedrine cause vasoconstriction and lead to an increase in blood pressure.

The nurse should assess the patient’s dietary habits and discuss any problems regarding intake. The patient’s height and weight should be recorded, and any recent weight changes evaluated.

CKD is a lifelong illness. The chronicity of kidney disease and the long-term treatment period affect virtually every area of a person’s life, including family relationships, social and work activities, self-image and emotional state. The nurse should assess the patient’s support systems.⁴⁷ It is important to recognise that people with CKD often have low levels of activity and nurses should try to encourage healthy activities.⁴⁸ The choice of treatment modality may be related to support systems available to the patient. Rather than simply focusing on clinical targets, nurses need to provide information and psychosocial and practical support to maximise the patient’s quality of life.⁴⁷

Planning

The overall goals are that the patient with CKD will: (1) demonstrate knowledge and ability to comply with the therapeutic regimen; (2) participate in decision making for the plan of care and future treatment modality; (3) demonstrate effective coping strategies; and (4) continue with activities of daily living within physiological limitations.

Nursing implementation

Health promotion

Individuals at risk of CKD must be identified. These include people with a history (or a family history) of kidney disease, hypertension, diabetes mellitus and repeated urinary tract infection. These individuals should have regular check-ups, including serum urea and creatinine levels and calculation of estimated GFR, along with a routine urinalysis. People with diabetes need to have their urine checked for microalbuminuria if routine urinalysis is negative for protein. They should be asked to report any changes in urine appearance (colour, odour), frequency or volume to their healthcare provider. If a patient must be prescribed a potentially nephrotoxic drug, it is important to monitor kidney function with serum creatinine and urea levels.

Individuals identified as at risk need to take measures to prevent or delay the progression of CKD, particularly by modifying behavioural and biomedical risk factors.⁴⁹ These include weight reduction, increasing exercise, smoking cessation, glycaemic control for patients with diabetes (see Ch 48), blood pressure control, and early and definitive treatment of urinary tract infections.

Acute intervention

Most of the care of the patient with CKD occurs on an outpatient basis, but in-hospital care will be required for the management of complications and for kidney transplantation (if done).

Ambulatory and home care

The specific nursing management of the patient with CKD is detailed in NCP 46-1. It is important to teach the patient and family about the required diet, drugs and follow-up healthcare because these are the responsibility of the patient (see Box 46-4).⁵⁰ Patients should check their weight daily, learn to take their blood pressure daily and be able to identify the signs and symptoms of fluid overload, hyperkalaemia and other electrolyte imbalances. The patient and family must understand the importance of strict dietary adherence. The dietician should meet with the patient and family on a regular basis for diet planning. A diet history and consideration of cultural variations will facilitate diet planning and adherence.

BOX 46-4 Chronic kidney disease

PATIENT & FAMILY TEACHING GUIDE

Include the following information in the teaching plan:

1. Necessary dietary (protein, sodium, potassium, phosphate) and fluid restrictions.

2. Difficulties in modifying diet and fluid intake.

3. Signs and symptoms of electrolyte imbalance, especially high potassium.

4. Alternative ways of reducing thirst, such as sucking on ice cubes, lemon or hard lollies.

5. Rationales for prescribed drugs and common side effects. Examples:

• Phosphate binders (including calcium supplements used as phosphate barriers) should be taken with meals.

• Calcium supplements prescribed to treat hypocalcaemia directly should be taken on an empty stomach (but not at the same time as iron supplements).

• Iron supplements should be taken between meals.

6. The importance of reporting any of the following:

• weight gain greater than 2 kg

• increasing blood pressure

• shortness of breath

• oedema

• increasing fatigue or weakness

• confusion or lethargy.

7. Need for support and encouragement. Share concerns about lifestyle changes, living with a chronic illness and decisions about type of dialysis or transplantation.

The patient needs a complete understanding of the drugs, their dosages and common side effects. It may be helpful to make a list of the drugs and the times of administration to display in the home. The patient must be instructed to avoid certain over-the-counter drugs such as NSAIDs, magnesium-based laxatives and antacids. The patient should also be aware that pethidine and ACE inhibitors may be harmful due to renal insufficiency.

Motivating patients to assume the primary role in the management of their disease is essential. The period of conservative management provides an opportunity to evaluate each patient’s ability to manage the disease—this knowledge will be helpful when determining the treatment modality. The length of time that a patient can receive conservative therapy is highly variable and depends on the progression of CKD and the presence of other coexisting conditions. While the patient is receiving conservative therapy, the decision regarding future therapies should be made. This should be done before complications, such as mental status changes, bleeding, progressive neuropathies and fluid overload, occur. When conservative therapy is no longer effective, KRT (involving HD, PD or kidney transplantation) is the available treatment option.

The patient and family need a clear explanation of what is involved in KRT. If alternative treatments are presented early in the course of therapy, there will be an opportunity to consider choices for dialysis, transplantation and even the option for palliative care. The opportunity for home HD needs to be discussed depending on availability in the community. In the best of circumstances, patients can receive a transplant before ever having to start dialysis, thus avoiding the need to begin dialysis. Even though transplantation offers the best therapeutic management for patients with kidney failure, the critical shortage of donor organs has limited this treatment option. Providing information about the treatment options will allow the patient to be active in the decision-making process and gives a sense of control over life-altering decisions. The patient should be informed that if dialysis is chosen, the option of transplantation still remains; and if a transplanted organ fails, the patient can return to dialysis. The patient should also be informed that re-transplantation may be an option.

It is important to respect the patient’s choice not to receive treatment. Many times, patients will initiate the conversation about palliative care themselves. The discussion needs to focus on moving from the curative approach to promotion of comfort care and consideration for hospice care. The nurse should listen to the patient and family, allowing them to do most of the talking and paying special attention to their hopes and fears.³³ (Palliative and end-of-life care is discussed in Ch 9.)

Evaluation

The expected outcomes for the patient with CKD are presented in NCP 46-1.

DIALYSIS

Dialysis is the movement of fluid and molecules across a semipermeable membrane from one compartment to another. Clinically, dialysis is a technique in which substances move from the blood through a semipermeable membrane and into a dialysis solution (dialysate). It is used to correct fluid and electrolyte imbalances and to remove waste products in kidney failure. It can also be used to treat drug overdoses. The two methods of dialysis available are peritoneal dialysis and haemodialysis (see Table 46-10). In PD the peritoneal membrane acts as the semipermeable membrane. In HD an artificial membrane (usually made of cellulose-based or synthetic materials) is used as the semipermeable membrane and is in contact with the patient’s blood.⁵¹

TABLE 46-10 Comparison of peritoneal dialysis and haemodialysis

CAPD, continuous ambulatory peritoneal dialysis.

Dialysis is begun when the patient’s uraemia can no longer be adequately managed conservatively. Generally, dialysis is initiated when the eGFR (or creatinine clearance) is less than 15 mL/min/1.73 m². This criterion can vary widely in different clinical situations and the treating doctor will determine when to start dialysis based on the patient’s clinical status. Certain uraemic complications, including encephalopathy, neuropathies, uncontrolled hyperkalaemia, pericarditis and accelerated hypertension, indicate a need for immediate dialysis.

General principles of dialysis

Solutes and water move across the semipermeable membrane from the blood to the dialysate or from the dialysate to the blood in accordance with concentration gradients. The principles of diffusion, osmosis and ultrafiltration are involved in dialysis (see Fig 46-7). Diffusion is the movement of solutes from an area of higher concentration to an area of lower concentration. During dialysis, urea, creatinine, uric acid and electrolytes (potassium, phosphate) move from the blood to the dialysate, with the net effect of lowering their concentrations in the blood. RBCs, WBCs and plasma proteins are too large to diffuse through the pores of the membrane. Bacteria and viruses that may be present in the dialysate are too large to migrate through the pores into the blood.

Figure 46-7 Osmosis and diffusion across a semipermeable membrane. RBC, red blood cell; WBC, white blood cell.

Osmosis is the movement of fluid from an area of lower to an area of higher concentration of solutes. Glucose is added to the dialysate and creates an osmotic gradient across the membrane, pulling excess fluid from the blood.

Ultrafiltration (water and fluid removal) results when there is an osmotic gradient or pressure gradient across the membrane. In PD, excess fluid is removed by increasing the osmolality of the dialysate (osmotic gradient) by the addition of glucose. In HD, the gradient is created by increasing pressure in the blood compartment (positive pressure) or decreasing pressure in the dialysate compartment (negative pressure). Extracellular fluid moves into the dialysate because of the pressure gradient. The excess fluid is removed by creating a pressure differential between the blood and the dialysate solution with a combination of positive pressure in the blood compartment or negative pressure in the dialysate compartment.

Peritoneal dialysis

Although PD was first used in 1923, it did not come into widespread use for chronic treatment until the 1970s with the development of soft, pliable peritoneal solution bags and the introduction of the concept of continuous PD.⁵² In Australia, approximately 25% of patients receiving dialysis treatments are on PD. In New Zealand this percentage is higher at 49%, representing 79% of those who perform their dialysis at home.²² In recent years the use of PD to treat CKD has decreased in the US to approximately 10% of patients.

CATHETER PLACEMENT

Peritoneal access is obtained by inserting a catheter through the anterior abdominal wall. The prototype of the catheter that is used was developed by Tenckhoff in 1968 and was made of silicone rubber tubing (see Fig 46-8). The catheter is about 60 cm long and has two Dacron cuffs on the subcutaneous and peritoneal portions that act as anchors and prevent the migration of microorganisms down the shaft from the skin (see Fig 46-9). Within a few weeks, fibrous tissue grows into the Dacron cuff, holding the catheter in place and preventing bacterial penetration into the peritoneal cavity. The tip of the catheter rests in the peritoneal cavity and has many perforations spaced along the distal end of the tubing to allow fluid to flow in and out of the catheter.

Figure 46-8 Tenkhoff catheter used in peritoneal dialysis.

Figure 46-9 A, Peritoneal catheters used for peritoneal dialysis. B, Bent neck, curl catheters. C, Disc catheters.

The technique for catheter placement varies. Although it is possible to place a permanent catheter in the peritoneal cavity at the bedside with a trocar, it is usually done using a surgical technique so that its placement can be directly visualised, minimising potential complications. Preparation of the patient for catheter insertion includes emptying the bladder and bowel, weighing the patient and obtaining a signed consent form.

In the non-surgical (bedside) approach, an area approximately 2 cm below the umbilicus is numbed with a local anaesthetic and a small stab wound is made. A stylet is inserted and the abdomen is distended with dialysis solution. The catheter is then placed into the peritoneal cavity. When the patient feels pressure in the rectal area and has the urge to defecate, the catheter is in place.

In the surgical approach, a midline umbilical incision is made and a small puncture is made to one side and below this incision. The distal end of the catheter is placed in the peritoneum and it is tunnelled under the skin to the puncture site. The tunnel helps prevent peritonitis. After the catheter is inserted, the skin is cleaned with an antiseptic solution and a sterile dressing is applied. Complications of catheter insertion include perforation of the bladder, the bowel or a blood vessel, and the introduction of bacteria.

The catheter is connected to a sterile tubing system and secured to the abdomen with tape. The catheter is irrigated immediately with heparinised dialysate (usually 500 mL) to clear blood and fibrin from it. Prophylactic antibiotics may also be instilled. The irrigations may continue for 12–24 hours using small volumes of dialysate. This procedure helps prevent catheter occlusion that can lead to poor drainage and inflow. Catheter placement is usually same-day surgery and the patient is discharged home with a sterile dressing covering the PD catheter. The patient needs instructions on keeping the dressing dry, avoiding accidentally pulling the catheter and receiving follow-up care.

Before the start of PD, it is preferable to allow a waiting period of 7–14 days for proper sealing of the catheter and for tissue to grow into the cuffs. However, some centres start dialysis 5–7 days after catheter insertion. About 4–6 weeks after catheter implantation, the exit site should be clean, dry and free of redness and tenderness (see Fig 46-10). Once the catheter incision site is healed, the patient may shower and then pat the catheter and exit site dry. Daily catheter care includes the application of an antiseptic solution and a clean dressing, as well as examination of the catheter site for signs of infection. Hand-washing is critical before exit site care.

Figure 46-10 Peritoneal catheter exit site.

DIALYSIS SOLUTIONS AND CYCLES

Commercial PD solutions are available from 500 mL to 3000 mL, containing varying levels of glucose concentrations ranging between 0.5% and 4.25%. The choice of exchange volume is primarily determined by the size of the peritoneal cavity. A larger person may tolerate a 3-L exchange volume without any difficulty, whereas an average-size person usually tolerates a 2-L exchange. Patients with a smaller body, with pulmonary compromise (the added pressure of the large volume may precipitate respiratory difficulty) or with inguinal hernias require a smaller exchange volume. The glucose acts as an osmotic agent. Higher concentrations remove water; lower concentrations are used when the patient is dehydrated and there is a need to conserve water. The electrolyte composition is similar to that of plasma. The dialysis solution is warmed to body temperature using dry heat to increase peritoneal clearance, prevent hypothermia and enhance comfort.

Ultrafiltration (fluid removal) during PD depends on osmotic forces, with dextrose being the most commonly used osmotic agent in PD solutions. However, the problems arising from high rates of peritoneal glucose absorption—such as obesity, hypertriglyceridaemia and difficult control of blood glucose in the diabetic patient—and long-term peritoneal membrane dysfunction mean that alternative dialysate solutions need to be used. Alternatives include icodextrin and amino acid solutions. Icodextrin is a commercially available preparation that is an iso-osmolar solution and induces ultrafiltration by its oncotic effect. Amino acid solutions are primarily used for patients requiring nutritional supplementation.

The three phases of the PD cycle are inflow (fill), dwell (equilibration) and drain.⁵¹ These three phases are called an exchange. The patient dialysing at home will receive about four exchanges per day. An acutely ill hospitalised patient may receive 12–24 exchanges per day. During inflow, a prescribed amount of solution, usually 2 L, is infused through an established catheter over about 10 minutes. The flow rate may be decreased if the patient has pain. After the solution has been infused, the inflow clamp is closed before air enters the tubing.

The next part of the cycle is the dwell phase, or equilibration, during which diffusion and osmosis occur between the patient’s blood and the peritoneal cavity. The duration of the dwell time can be 20– 30 minutes to 8 hours or more depending on the method of PD. Draining takes 15–30 minutes and may be facilitated by gently massaging the abdomen or changing position. The cycle starts again with the infusion of another 2 L of solution. For manual PD, a period of about 30–50 minutes is required to complete an exchange.

PERITONEAL DIALYSIS SYSTEMS

Two types of PD currently being used are automated peritoneal dialysis (APD) and continuous ambulatory peritoneal dialysis (CAPD).

Automated peritoneal dialysis

An automated device called a cycler is used to deliver the dialysate for APD (see Fig 46-11). The automated cycler times and controls the fill, dwell and drain phases. The machine cycles four or more exchanges per night with 1–2 hours per exchange. Alarms and monitors are built into the system to make it safe for the patient to dialyse while sleeping. The patient disconnects from the machine in the morning and usually leaves fluid in the abdomen during the day. One to two daytime manual exchanges may also be prescribed to ensure adequate dialysis. It is difficult to achieve the required solute and fluid clearance with solely night-time APD. The cycler is about the size of a DVD player and with longer tubing greater mobility is possible.

Figure 46-11 Automated peritoneal dialysis can be used while the patient is sleeping at night or for hospitalised patients who require frequent exchange.

Continuous ambulatory peritoneal dialysis

CAPD is more laborious and is done while the patient is awake during the day (see Fig 46-12). Exchanges are carried out manually by exchanging 1.5–3 L of peritoneal dialysate at least four times daily, with dwell times averaging 4 hours. For example, one schedule starts the exchanges at 7 am, 12 noon, 5 pm and 10 pm. In this procedure the person instils 2–3 L of dialysate from a collapsible plastic bag into the peritoneal cavity through a disposable plastic tube.

Figure 46-12 Infusion period for a continuous ambulatory peritoneal dialysis patient.

Technical advances in CAPD systems allow the bag and line to be disconnected after the instillation of the fluid, decreasing the risk of peritonitis. After the equilibration period, the line is reconnected to the catheter, the dialysate (effluent) is drained from the peritoneal cavity and a new 2- to 3-L bag of dialysate solution is infused. It is critical in PD to maintain aseptic technique to avoid peritonitis. Several tubing connections and devices are commercially available to help in maintaining an aseptic system.

COMPLICATIONS OF PERITONEAL DIALYSIS

Exit site infection

Infection of the peritoneal catheter exit site is most commonly caused by Staphylococcus aureus or Staphylococcus epidermidis (from skin flora).⁵³ Superficial exit site infections caused by these organisms are generally resolved with antibiotic therapy. Clinical manifestations of an exit site infection include redness at the site, tenderness and drainage. If not treated immediately, subcutaneous tunnel infections usually result in abscess formation and may cause peritonitis, necessitating catheter removal.

Peritonitis

Peritonitis results from contamination of the dialysate or tubing or from progression of an exit site or tunnel infection. Most frequently peritonitis occurs because of improper technique in making or breaking connections for exchanges. Less commonly, peritonitis results from bacteria in the intestine crossing over into the peritoneal cavity. Peritonitis is usually caused by S. aureus or S. epidermidis. The primary clinical manifestation of peritonitis is a cloudy peritoneal effluent that has a WBC count of over 100 cells/μL (particularly neutrophils). GI manifestations may also be present, including diffuse abdominal pain, diarrhoea, vomiting, abdominal distension and hyperactive bowel sounds. Fever may or may not be present. Cultures, Gram stain and a WBC count differential of the peritoneal effluent are used to confirm the diagnosis of peritonitis. Antibiotics can be given by mouth, IV or intraperitoneally. The patient is usually treated on an outpatient basis.⁵³ Repeated infections may require the removal of the peritoneal catheter and termination of PD. The formation of adhesions in the peritoneum can result from repeated infections and interferes with the peritoneal membrane’s ability to act as a dialysing surface.

Abdominal pain

Although not severe, pain is a common complication caused by the low pH of the dialysate solution, peritonitis, intraperitoneal irritation (which usually subsides in 1–2 weeks) and placement of the catheter. Pain can also occur when the tip of the catheter touches the bladder, bowel or peritoneum. A change in the position of the catheter should correct this problem. Accidental infusion of air or infusing the dialysate too rapidly may cause referred pain in the shoulder. If the infusion rate is decreased, the pain usually subsides.

Outflow problems

If the outflow is less than 80% of inflow immediately after catheter placement, it may be caused by a kink in the tunnel segment of the catheter, omentum wrapped around the catheter or migration of the catheter out of the pelvic region. Persistent outflow problems may require radiological or surgical manipulation of the catheter. Outflow problems after the catheter has settled into place are often the result of a full colon. Bowel evacuation frequently relieves the problem.

Hernias

Because of increased intraabdominal pressure secondary to the dialysate infusion, hernias can develop in predisposed individuals (e.g. multiparous women, older men). However, in most situations after hernia repair, PD can be resumed after several days using small dialysate volumes and by keeping the patient supine.

Lower back problems

Increased intraabdominal pressure can cause or aggravate lower back pain. The lumbosacral curvature is increased by intraperitoneal infusion of dialysate. Orthopaedic binders and a regular exercise program for strengthening the back muscles are beneficial for some patients.

Bleeding

Effluent drained after the first few exchanges may be pink or slightly bloody because of the trauma of catheter insertion. Bloody effluent over several days or the new appearance of blood in the effluent can indicate active intraperitoneal bleeding. If this occurs, the blood pressure and haematocrit should be checked. Blood may also be present in the effluent of women who are menstruating or ovulating, and this requires no intervention.

Pulmonary complications

Atelectasis, pneumonia and bronchitis may occur from repeated upward displacement of the diaphragm, resulting in decreased lung expansion. The longer the dwell time, the greater the likelihood of pulmonary problems. Frequent repositioning and deep-breathing exercises can help. When lying in bed, elevation of the head of the bed may prevent these problems.

Protein loss

The peritoneal membrane is permeable to plasma proteins, amino acids and polypeptides. These substances are lost in the dialysate fluid. The amount of loss is usually about 0.5 g/L of dialysate drainage, but can be as high as 10–20 g per day. This loss may increase to as much as 40 g per day during episodes of peritonitis as the membrane becomes more permeable. Unresolved peritonitis is associated with exaggerated protein loss that can result in malnutrition and may indicate the need to terminate PD temporarily or, on occasion, permanently.⁵¹

Carbohydrate and lipid abnormalities

Dialysate glucose is absorbed via the peritoneum and may be as much as 100–150 g per day. Continuous absorption of glucose results in increased insulin secretion and increased plasma insulin levels. The hyperinsulinaemia stimulates hepatic production of triglycerides.

EFFECTIVENESS OF AND ADAPTATION TO CHRONIC PERITONEAL DIALYSIS

The technique is associated with a short training program, independence and ease of travelling.⁵⁴ Learning the self-management skills required to undertake PD is usually accomplished in a 3–7-day training program. Mortality rates are about equal between in-centre HD patients and PD patients for the first few years or possibly even a little lower for patients receiving PD. However, after about 2 years, mortality rates for patients receiving PD are higher, especially for the elderly with diabetes and patients with a prior history of cardiovascular disease. There are fewer dietary restrictions and greater mobility is possible than with conventional HD. The major disadvantage is the possibility of developing peritonitis. As further improvements in techniques are made (e.g. improved connecting and sterilising devices, in-line filters, improved catheters), the incidence of peritonitis should decrease.⁵⁴

The primary advantage of PD is its simplicity and that it is a home-based program allowing the patient to be in control. There is no need for special water systems, and equipment set-up is relatively simple. PD is especially indicated for the individual who has vascular access problems or responds poorly to the haemodynamic stresses of HD (e.g. the older adult patient with diabetes and cardiovascular disease). Peritoneal function tests to measure clearances for each exchange over a 24-hour period are done to measure PD adequacy. Urea kinetic modelling is also done to calculate the total clearance of urea (from both dialysate and urine).

Haemodialysis

In 1943 in The Netherlands Willem Kolff performed the first successful dialysis on a human being with the use of a rotating-drum dialyser. He initiated dialysis treatment in the US in 1948.⁵¹ Haemodialysis began in the early 1960s in Australia and in the later 1960s in New Zealand. Tremendous technological advances have been made in HD since the 1940s, allowing for safer, shorter treatments using sophisticated equipment.

VASCULAR ACCESS SITES

Obtaining vascular access is one of the most difficult problems associated with HD. To carry out HD, a very rapid blood flow is required and access to a large blood vessel is essential. The types of vascular access in current use include arteriovenous fistulas (AVFs) and arteriovenous grafts (AVGs), temporary and semipermanent catheters, and subcutaneous ports (see Fig 46-13).

Figure 46-13 Vascular access for haemodialysis. A, External shunt. B, Internal arteriovenous fistula. C, Internal arteriovenous graft.

Arteriovenous fistulas and grafts

A subcutaneous AVF is created most commonly in the forearm with an anastomosis between an artery (usually radial or ulnar) and a vein (usually cephalic; see Fig 46-13, B). The fistula allows arterial blood to flow through the vein. The arterial blood flow is essential to provide the rapid blood flow required for HD. The increased pressure of the arterial blood flow through the vein makes the vein dilate and become tough, making it amenable to repeated venipuncture in approximately 4–6 weeks, although it is recommended that the AVF be created at least 3 months prior to the initiation of HD. The vein is accessed using two large-gauge needles.

Native fistulas (formed out of the patient’s own blood vessels, rather than synthetic material) have the best overall patency rates and least number of complications (e.g. thrombosis, infection) of all vascular accesses and are commonly used throughout both New Zealand and Australia.⁵⁵ Ideally an AVF should be attempted first, before an AVG. However, AVFs are suitable only for patients with relatively healthy blood vessels—they are more difficult to create in patients with a history of severe hypertension, peripheral vascular disease, diabetes mellitus, prolonged IV drug use or previous multiple IV procedures in the forearm. For these individuals, an AVG is usually required.

AVGs are made of synthetic materials (polytetrafluoroethylene [PTFE], Teflon) and form a ‘bridge’ between the arterial and venous blood supplies. Grafts are placed under the skin and are surgically anastomosed between an artery (usually brachial) and a vein (usually antecubital; see Fig 46-13, C). An interval of 2–4 weeks is usually necessary to allow the graft to heal, but some centres may use it earlier. The graft, like the fistula, is accessed using two large-gauge needles, and the graft material is self-healing, closing over any puncture site with sufficient pressure to stop the bleeding when needles are removed. Because grafts are made of artificial materials, they can become infected easily and are thrombogenic.

The needles used for haemodialysis are large bore, usually 14- to 16-gauge and are inserted into the fistula or graft to obtain vascular access. One needle is placed to pull blood from the circulation to the HD machine, and the other needle is used to return the dialysed blood to the patient. The needles are attached via tubing to dialysis lines. Normally, a thrill can be felt by palpating the area of anastomosis and a bruit can be heard with a stethoscope. The bruit and thrill are created by arterial blood rushing into the vein.

Blood pressure testing, insertion of IVs and venipuncture should not be performed on the affected extremity. These special precautions are taken to prevent infection and clotting of the vascular access. AVFs are much less likely to clot and become infected than grafts. Thrombosis in AVGs is common but can often be corrected with interventional radiology techniques or a surgical procedure. AVGs can cause the development of distal ischaemia (steal syndrome) because too much of the arterial blood is being shunted or ‘stolen’ from the distal extremity. This is usually seen soon after surgery and may require surgical correction. Aneurysms can also develop at the fistula site and can rupture if left untreated. This is a life-threatening situation. AVG infections are not uncommon and immediate treatment is essential to salvage the graft and prevent bacteraemia. Severe AVG infections may necessitate graft removal. Vascular access can be difficult to obtain for patients with ESKD. Protection of the vascular access site is of paramount importance.

Temporary vascular access

In some situations when immediate vascular access is required, percutaneous cannulation of the internal jugular or femoral vein is performed.⁵¹ In the past, the subclavian vein was often cannulated, but the central stenosis that can occur with this approach has made it the option of last resort. A flexible Teflon, silicone rubber or polyurethane catheter (e.g. Vas Cath) is inserted into one of these large veins at the bedside and provides access to circulation without surgery (see Fig 46-14). The catheters usually have a double external lumen with an internal septum separating the two internal segments. One lumen is used for blood removal and the other for blood return. Temporary catheters in the jugular or subclavian veins can be left in place for 1–3 weeks, not to exceed 3 weeks (see Fig 46-15, B). Femoral vein cannulas can remain in place for up to 1 week, but necessitate careful monitoring usually in an intensive care unit setting, since the patient is often confined to the bed.

Figure 46-14 Temporary double-lumen vascular access catheter for acute haemodialysis. A, Soft, flexible double-lumen tube is attached to a Y hub. B, Blood is withdrawn continuously through the outer lumen upstream and returned through the inner lumen downstream, thus reducing circulation. The distance between the arterial intake and the venous return lumina typically provides recirculation rates of 5% or less.

Figure 46-15 A, Right internal jugular placement for a tunnelled, cuffed semipermanent catheter. B, Temporary haemodialysis catheter in place. C, Long-term cuffed haemodialysis catheter

(B and C, courtesy Dr. Stephen Van Voorst, MD.)

Jugular vein cannulation is associated with a low incidence of thrombosis (see Fig 46-15, A). This is the primary reason this method is preferred over subclavian cannulation. In addition to vessel thrombosis and stenosis, subclavian vein cannulation has been associated with pneumothorax, brachial plexus neuropathies and haemothorax. Both types of catheter placements pose the risk of infection. Disadvantages of femoral vessel cannulisation include the following: (1) the catheter can remain in place only a short time; (2) the location encourages catheter kinking; and (3) the groin is not a clean site. Potential complications of femoral catheterisation are femoral vein thrombosis with pulmonary emboli (especially if the treatment is prolonged), infections, immobility and inadvertent blood vessel punctures with haematoma formation. The patient must be on bed rest while the femoral catheter is in place to prevent trauma to the vessel.

For all temporary catheters, no drugs should be administered or blood withdrawn via the catheter by non-dialysis staff. This is to minimise the risk of infection, catheter loss and accidental injection of heparin. Trained dialysis staff will instil heparin into the lumens of the catheter at the end of each treatment to ensure patency and withdraw it before the next treatment. Should patency be incapacitated, as shown by an inability to withdraw blood, instillation of a medication as prescribed by specialty staff to restore function may be necessary (e.g. Urokinase). Commonly a transparent dressing is applied over the catheter so that direct visualisation of the insertion site can be observed. Semipermanent, soft, flexible long-term cuffed haemodialysis catheters are being used more often because these catheters provide temporary access while awaiting fistula placement and development or as long-term access when other forms of access have failed. This type of catheter exits on the upper chest wall and is tunnelled subcutaneously to the internal or external jugular vein (see Fig 46-15, C). The catheter tip rests in the right atrium. It has one or two subcutaneous Dacron cuffs that prevent infection from tracking along the catheter and anchor the catheter, thus eliminating the need for sutures.

Advance planning is essential for management of the patient with kidney failure who is approaching end-stage disease and dialysis. Patients who are referred to a nephrology team late have a higher mortality rate compared to those referred early. Timely referral allows for targeted risk factor management, as well as evaluation and consideration of the best possible arteriovenous access for HD and preparation for PD.

DIALYSERS

The dialyser is a long plastic cartridge that contains thousands of parallel hollow tubes or fibres. The fibres are the semipermeable membrane made of cellulose-based or other synthetic materials. The blood is pumped into the top of the cartridge and dispersed into all of the fibres. Dialysis fluid (dialysate) is pumped into the bottom of the cartridge and bathes the outside of the fibres with dialysis fluid. Ultrafiltration, diffusion and osmosis occur across the pores of this semipermeable membrane. When the dialysed blood reaches the end of the thousands of semipermeable fibres, it converges into a single tube that returns it to the patient. Dialysers available differ in regard to surface area, membrane composition and thickness, clearance of waste products and removal of fluid.

PROCEDURE FOR HAEMODIALYSIS

To initiate chronic dialysis in a patient with an AVG or AVF, two needles are placed in the fistula or graft. If the patient has a catheter, the two blood lines are attached to the two catheter lumens (see Fig 46-16). The needle closest to the fistula or the red catheter lumen is used to pull blood from the patient and send it to the dialyser with the assistance of a blood pump. The dialyser and blood lines are usually primed with up to 1000 mL of saline solution to eliminate air from the system. Heparin is added to the blood as it flows into the dialyser because whenever blood contacts a foreign substance it has a tendency to clot. When the blood enters the extracorporeal circuit, it is propelled through the top of the dialyser by a blood pump at a flow rate of 200–500 mL per minute, while the dialysate (warmed to body temperature) circulates in the opposite direction at a rate of 300–900 mL per minute. Blood is returned from the dialyser to the patient through the second needle or through the blue catheter lumen.

Figure 46-16 Components of a haemodialysis system. Blood is removed via a needle inserted in a fistula or via catheter lumen. It is propelled to the dialyser by a blood pump. Heparin is infused either as a bolus pre-dialysis or through a heparin pump continuously to prevent clotting. Dialysate is pumped in and flows in the opposite direction of the blood. The dialysed blood is returned to the patient through a second needle or catheter lumen. Old dialysate and ultrafiltrate are drained and discarded.

In addition to the dialyser, there is a dialysate delivery and monitoring system. This system pumps the dialysate through the dialyser countercurrent to the blood flow. Adjustments can be made for ultrafiltration by creating a positive pressure on the blood side or a negative pressure on the dialysate side, or by a combination of both. The newest dialysis delivery systems have ultrafiltration controllers that equalise negative and positive pressures for the removal of a precise amount of fluid per hour. The dialysis system has alarm systems to warn of blood leaking into the dialysate or air leaking into the blood; alterations in dialysate temperature, concentration or pressure; and extremes in blood pressure readings.

Dialysis is terminated by flushing the dialyser with saline solution to return all blood through the access site. The needles are then removed from the patient and firm pressure is applied to the venipuncture sites until the bleeding stops. On occasion the access site can begin to bleed again. If this occurs, pressure should be reapplied but not so firmly that flow is occluded because this could cause thrombosis. For patients with a catheter, the blood lines are clamped and removed from the catheter lumens.

Before beginning treatment, the nurse must complete an assessment that includes fluid status (weight, blood pressure, peripheral oedema, lung and heart sounds), condition of vascular access, temperature and general skin condition. The difference between the last post-dialysis weight and the present pre-dialysis weight determines the ultrafiltration or the amount of weight to be removed. Ideally, no more than 1–1.5 kg should be gained between treatments to avoid causing hypotension associated with the removal of larger volumes of fluid. Many patients gain 2–3 kg between treatments and this volume usually can be removed if their blood pressure is not labile. While the patient is on dialysis, vital signs should be taken at least every 30–60 minutes because rapid changes may occur in the blood pressure.

Most maintenance dialysis units use reclining chairs that allow for elevation of the feet if hypotension develops. Most people sleep, read, talk or watch television during dialysis. Treatments usually last 3–5 hours and are done three times per week to achieve adequate clearance and maintain fluid balance.

Settings for haemodialysis

HD can be done in an inpatient (hospital) or outpatient (clinic, hospital or satellite) setting. Inpatient dialysis is predominantly used for treating hospitalised patients. In outpatient dialysis the patient comes to the unit for treatment. The patient may choose to do self-care with back-up support from trained personnel if needed. Self-care patients put in the dialysis needles, set up the machine and monitor the course of the treatment. Community-based or satellite dialysis units are increasing in all areas of Australia and New Zealand.²² This is in part due to the high incidence of ESKD in Indigenous people who live in remote or regional areas.

HD can also be done at home (see Fig 46-17). In Australia and New Zealand approximately 25% of all patients perform their own HD treatment at home.²² In the US, this figure is less than 1.5%.⁵⁶ Daily home HD has shown some promise in the overall improvement of patient status: fluid management, control of blood pressure, improved nutritional status and better uraemic clearance.⁵⁷ In Australia and New Zealand, HD is also performed overnight by patients in their own homes.⁵⁸ However, this is not a method of treatment often supported by dialysis centres. For home dialysis, PD tends to be the treatment of choice because it is less technically demanding, requires less specialised equipment and no water treatment system is needed.

Figure 46-17 Home haemodialysis is growing in popularity and machines are more compact.

COMPLICATIONS OF HAEMODIALYSIS

Hypotension

Hypotension during HD primarily results from rapid removal of vascular volume (hypovolaemia), decreased cardiac output and decreased systemic intravascular resistance. The drop in blood pressure during dialysis may precipitate light-headedness, nausea, vomiting, seizures, vision changes and chest pain from cardiac ischaemia. The usual treatment for hypotension includes decreasing the volume of fluid being removed and infusion of 0.9% saline solution (100–300 mL). If a patient experiences recurrent hypotensive episodes, a reassessment of dry weight and blood pressure drugs may be needed. Blood pressure drugs should be withheld before dialysis if there are frequent episodes of hypotension during dialysis.

Muscle cramps

Painful muscle cramps are a common problem. The pathogenesis of muscle cramps in haemodialysis is poorly understood. Factors associated with their development include hypotension, hypovolaemia, high ultrafiltration rate (large interdialytic weight gain) and use of low-sodium dialysis solution. Cramps are more frequently seen in the first month after initiation of dialysis than in the subsequent period. Treatment includes reducing the ultrafiltration rate and administration of fluids (saline, glucose, mannitol). Hypertonic saline is not recommended since the sodium load can be problematic; hypertonic glucose administration is preferred.

Loss of blood

Blood loss may result from blood not being completely rinsed from the dialyser, accidental separation of blood tubing, dialysis membrane rupture or bleeding after the removal of needles at the end of dialysis. If a patient has received too much heparin or has clotting problems, there can be significant post-dialysis bleeding. It is essential to rinse back all blood, to monitor heparinisation closely to avoid excess anticoagulation and to hold firm but non-occlusive pressure on access sites until the risk of bleeding has passed.

Hepatitis

The causes of hepatitis B and C in dialysis patients include blood transfusions and the lack of adherence to precautions used to prevent the spread of infection. Since blood is now screened for hepatitis B and C, blood is an unlikely source of infection. IV drug abuse and unprotected sex can also contribute to the incidence of hepatitis in the dialysis population. (Hepatitis is discussed in more detail in Ch 43.)

The incidence of hepatitis B has decreased with frequent testing for hepatitis B surface antigen in patients, isolation of dialysis patients who are positive for hepatitis B, and the use of disposable equipment, the hepatitis B vaccine and infection control precautions. All patients and personnel in dialysis units should receive hepatitis B vaccine.

Hepatitis C is responsible for the majority of cases of hepatitis in dialysis patients. The Kidney Disease Improving Global Outcomes (KDIGO) guidelines do not recommend isolating HD patients who have hepatitis C.⁵⁹ Standard precautions are mandated in the care of these patients to protect patients and staff. (Infection control precautions are discussed in Ch 12.) Currently, no vaccine is available for hepatitis C.

Sepsis

Sepsis is most often related to infections of vascular access sites. Bacteria can also be introduced during the dialysis treatment as a result of poor technique or interruption of blood tubing or dialyser membranes. Bacterial endocarditis can occur because of the frequent and prolonged access to the vascular system. Aseptic technique is essential to prevent this problem. Nurses must monitor patients for signs and symptoms of sepsis, such as fever, hypotension and an elevated WBC count.

Disequilibrium syndrome

Disequilibrium syndrome develops as a result of very rapid changes in the composition of the extracellular fluid. Urea, sodium and other solutes are removed more rapidly from the blood than from the cerebrospinal fluid and the brain. This creates a high osmotic gradient in the brain, resulting in the shift of fluid into the brain, causing cerebral oedema. Manifestations include nausea, vomiting, confusion, restlessness, headaches, twitching and jerking, and seizures. The rapid changes in osmolality may cause muscle cramps and worsen hypotension. Treatment consists of slowing or stopping dialysis and infusing hypertonic saline solution, albumin or mannitol to draw fluid from the brain cells back into the systemic circulation. It is more commonly observed in the initial treatment of a patient when the serum urea level is high. First dialysis treatment sessions are purposely short with limited total solute removal to prevent this rare syndrome.

EFFECTIVENESS OF AND ADAPTATION TO HAEMODIALYSIS

HD is still an imperfect technique for treating ESKD. It cannot fully replace the metabolic and hormonal functions of the kidneys. It can ease many of the symptoms of CKD and, if started early, can prevent certain complications. It does not alter the rate of development of cardiovascular disease and the related high mortality rate.

The yearly death rate of patients receiving maintenance dialysis is approximately 11%. The major reason for this is the increased proportion of older adults who are now receiving dialysis as maintenance therapy. The majority of deaths (49%) are caused by cardiovascular disease (myocardial infarction, cardiac arrest or stroke). Withdrawal of dialysis (27%) is the second leading cause of death, followed by infectious complications (14%).²²

Individual adaptation to maintenance HD varies considerably. Initially, many patients feel positive about the dialysis because it makes them feel better and keeps them alive, but there is often great ambivalence about whether it is worthwhile.⁶⁰ Dependence on a machine is a reality and some have dreams about being tied to the machine. In response to their illness, dialysis patients may demonstrate non-adherence, depression and suicidal tendencies. The primary nursing goals are to help patients to regain or maintain positive self-esteem and control of their lives and to continue to be productive in society. When a patient withdraws from dialysis, it is important to consult the palliative care team.⁶¹

Continuous renal replacement therapy

CRRT is an alternative or adjunctive method for treating AKI.⁶² It provides a means by which uraemic toxins and fluids are removed, while acid–base status and electrolytes are adjusted slowly and continuously from a haemodynamically unstable patient. The patients selected are usually those who do not respond to dietary interventions and pharmacological agents. CRRT is contraindicated if a patient has life-threatening manifestations of uraemia (hyperkalaemia, pericarditis) that require rapid resolution. CRRT can be used in conjunction with HD for continuous fluid removal. The principle of CRRT is to dialyse patients in a more physiologically consistent way over 24 hours, just like the kidneys.

Various types of CRRT are available, differentiated by whether arterial and/or venous access is required and if a blood pump is needed (see Table 46-11). There are several continuous therapies including continuous venovenous haemofiltration (CVVH), continuous venovenous haemodialysis (CVVHD), continuous venovenous haemodiafiltration (CVVHDF) and slow continuous ultrafiltration (SCUF). An intermittent therapy called sustained low-efficiency dialysis (SLED) is becoming more popular overseas. In Australia and New Zealand the most common techniques used are CVVHDF (62% of ICUs), followed by CVVH (35%) and CVVHD (3%). Replacement fluid is usually given pre-filter (pre-dilution) in most cases (94%).⁶³ Due to technological advances with automated and volumetric equipment that includes a blood pump, CRRT most commonly uses the venovenous approaches. These approaches are the focus of this discussion.

TABLE 46-11 Continuous renal replacement therapy

Vascular access for CVVH or CVVHD is achieved through the use of a double-lumen catheter (as used in HD and noted in Fig 46-14) placed in the femoral, jugular or subclavian vein. Venous access necessitates the use of a blood pump to propel blood through the circuit. A highly permeable, hollow fibre haemofilter removes plasma water and non-protein solutes, which are collectively termed ultrafiltrate. The ultrafiltration rate (UFR) may range from 0 to 500 mL per hour. Under the influence of hydrostatic pressure and osmotic pressure, water and non-protein solutes pass out of the filter into the extracapillary space and drain through the ultrafiltrate port into a collection device (drainage bag; see Fig 46-18). The remaining fluid continues through the filter and returns to the patient via the return port of the double-lumen catheter. While the ultrafiltrate drains out of the haemofilter, fluid and electrolyte replacements can be infused into the infusion port located after the filter as the blood returns to the patient. This fluid is designed to replace volume and solutes such as sodium, chloride, bicarbonate and glucose. It will also further dilute intravascular fluid, decreasing the concentration of unwanted solutes such as urea, creatinine and potassium. The infusion rate of replacement fluid is determined by the degree of fluid and electrolyte imbalance. Replacement fluid may also be infused into the infusion port before the haemofilter. This method allows for greater clearance of urea and can decrease filter clotting.

Figure 46-18 Basic schematic of continuous venovenous therapies. A blood pump is required to pump blood through the circuit. Replacement ports are used for instilling replacement fluids and can be given prefilter or postfilter. A dialysate port is used for infusing distillate. Regardless of modality, ultrafiltrate is drained via the ultrafiltration drain port.

Anticoagulation is needed to prevent blood clotting during CRRT. Heparin may be infused as a bolus at the initiation of CRRT or through the heparin infusion port before the haemofilter. Heparin dosage is based on the patient’s activated clotting time (ACT), partial prothrombin time (PTT) or prothrombin time (PT).

Several features of CRRT differ from HD:⁶²

Regardless of whether the modality is arteriovenous or venovenous, the approaches can be customised to the patient’s needs and have equivalent outcomes. The ultrafiltration therapies (slow continuous ultrafiltration [SCUF] and continuous venovenous ultrafiltration [CVVU]) are strictly for ultrafiltration or fluid removal. There is some convective loss of solutes, but no diffusion or osmosis is involved.

The haemofiltration therapies (continuous arteriovenous haemofiltration [CAVH] and CVVH) involve the introduction of replacement fluids. Large volumes of fluid may be removed hourly (200–800 mL) and then a portion of this fluid is replaced. The type of fluid replacement is dependent on the stability and individualised needs of the patient. Ultrafiltration and convective losses occur, and solute concentrations in the blood are diluted with the replacement fluid.

The haemodialysis therapies (continuous arteriovenous haemodialysis [CAVHD] and CVVHD) use dialysate. Peritoneal dialysate bags are attached to the distal end of the haemofilter and the fluid is pumped countercurrent to the blood flow. As in dialysis, diffusion of solutes and ultrafiltration via hydrostatic pressure and osmosis occur. This is an ideal treatment for a patient who needs both fluid and solute control but cannot tolerate the rapid fluid shifts associated with HD.

CRRT can be continued for as long as 30–40 days but the haemofilter should be changed about every 24–48 hours because of loss of filtration efficiency and the potential for clotting.^62,⁶⁴ The ultrafiltrate should be clear yellow, and serum specimens may be obtained for evaluation. If the ultrafiltrate becomes bloody or blood tinged, a possible rupture in the filter membrane should be suspected and treatment should be suspended immediately to prevent blood loss and infection.

The nurse responsible for the care of the patient with AKI who is receiving CRRT may be a critical care nurse or a nephrology nurse specialist, working in collaboration with other healthcare providers.⁶² Specific nursing interventions include obtaining weights and monitoring and documenting laboratory values daily to ensure adequate fluid and electrolyte balance. Hourly intake/output measurements, vital signs and haemodynamic status are essential. Although reductions in central venous pressure and pulmonary artery pressure are expected, there should be little change in mean arterial pressure or cardiac output. Patency of the CRRT system is assessed and maintained, and the patient’s vascular access site is cared for to prevent infection. Treatment is discontinued and the vascular access removed once the patient’s AKI is resolved or there is a decision to withdraw treatment due to patient deterioration.

Kidney transplantation

Major progress has been made in organ transplantation since the first kidney transplant was performed in 1954 in Boston between identical twins. The advances made in organ procurement and preservation, surgical techniques, tissue typing and matching, understanding of the immune system, immunosuppressant therapy, and prevention of and treatment for graft rejection have dramatically increased the success of organ transplantation.

The disparity between the supply and demand for organs is significant. In 2009, more than 1500 patients in Australia and New Zealand were waiting for a kidney transplant, but only 891 transplant operations were performed.^22,⁶⁵ Very few transplant recipients are from an Indigenous background.^22,⁶⁶ Living donor kidney transplants, from either living related donors (e.g. parent, sibling) or living unrelated donors (spouse, friend), are increasing due to the shortage of cadaveric organ donors in Australia and New Zealand. In 2009, 42% of all transplant operations in Australia and 55% in New Zealand were from living donors.^22,⁶⁵ Transplantation from a deceased donor usually requires a prolonged waiting period with differences depending on age, gender and race, as well as the availability of a matching blood type. Blood types B and O have the longest waiting times.⁶⁵

Kidney transplantation is extremely successful, with 1-year graft survival rates of more than 90% for cadaver transplants and 96% for live donor transplants, and patient survival more than 90% at 1 year following transplant.²² Over 80 people in Australia have had a functioning kidney transplant for more than 30 years. An advantage of kidney transplantation when compared with dialysis is that it reverses many of the physiological changes associated with renal insufficiency when normal kidney function is restored. It also eliminates the dependence on dialysis and the accompanying dietary and lifestyle restrictions. Transplantation is also less expensive than dialysis after the first year.

Payment for organs

CLINICAL PRACTICE

Situation

You are caring for Rosie, a 45-year-old woman, who has been receiving dialysis for nearly 10 years. She tells you she is on a waiting list for a kidney transplant but cannot deal with the long wait anymore. Recently she heard from a friend about the possibility of purchasing a kidney and having the transplant operation in India. She asks what you think about this option and what you would recommend.

RECIPIENT SELECTION

Appropriate recipient selection is important for a successful outcome. Candidacy is determined by a variety of medical and psychosocial factors that vary among transplant centres. A careful evaluation is completed in an attempt to identify and minimise potential complications after transplantation. Certain patients, particularly those with cardiovascular disease and diabetes mellitus, are considered high risk. Some patients who are approaching ESKD can receive a transplant before dialysis is required if they have a living donor (pre-emptive transplant). This approach is most advantageous for patients with diabetes, who have a much higher mortality rate on dialysis than non-diabetics.

Contraindications to transplantation include disseminated malignancies, refractory or untreated cardiac disease, chronic respiratory failure, extensive vascular disease, chronic infection and unresolved psychosocial disorders (e.g. non-adherence with medical regimens, alcoholism, drug addiction). The presence of hepatitis B or C is not a contraindication to transplantation.

Surgical procedures may be required before transplantation based on the results of the recipient evaluation. Coronary artery bypass or coronary angioplasty may be indicated for advanced coronary artery disease. Cholecystectomy may be necessary for patients with a history of gallstones, biliary obstruction or cholecystitis. On rare occasions, bilateral nephrectomies may be done for patients with refractory hypertension, recurrent urinary tract infections or grossly enlarged kidneys resulting from polycystic kidney disease. In general, the recipient’s own kidneys do not need to be removed prior to having a kidney transplant.

HISTOCOMPATIBILITY STUDIES

Histocompatibility studies, including human leucocyte antigen (HLA) testing and cross-matching, are discussed in Chapter 13.

DONOR SOURCES

Kidneys for transplantation may be obtained from compatible blood type deceased donors, blood relatives, emotionally related (close and distant) living donors (e.g. spouses, distant cousins, friends, etc.) and (potentially) altruistic living donors who are unknown to the recipient. Expanding the living donor pool is one of the best possibilities for decreasing the size of the waiting list and reducing waiting times for people needing a deceased donor.

Live donors

Live donors are required to undergo an extensive multidisciplinary evaluation to be certain that they are in good health and have no history of disease that would place them at risk for developing kidney failure or operative complications.⁶⁷ Psychosocial evaluations are done as well. Cross-matches are undertaken at the time of the evaluation and about a week before the transplant to ensure that no antibodies to the donor are present and that the antibody titre is below the allowed level. The advantages of a live donor kidney include better patient and graft survival rates regardless of histocompatibility match, immediate organ availability, immediate function because of minimal cold time (kidney out of body and not getting blood supply) and the opportunity to have the recipient in the best possible medical condition because the surgery is elective.

As a result of advances in technology and immunology, living donors do not necessarily need to be ABO compatible with the recipient. Plasmapheresis can be used to remove the antibodies to the incompatible blood group, and potent immunosuppression and immunomodulation with IV immune globulin dampen the response to the antibody. In addition, it is possible to have some antibodies to the donor HLA present and still proceed with the transplant. These antibodies can also be removed with plasmapheresis and the antibody level reduced with significant immunosuppression and immunomodulation. ABO incompatibility or the presence of antibody to the donor’s HLA complicates the transplant process. However, because the donor shortage is severe, complex measures are necessary to ensure that as many patients as possible are transplanted.

The donor will see a nephrologist for a complete history and physical examination, and laboratory and diagnostic studies. It is preferable that the donor’s nephrologist is not the same as the recipient’s nephrologist. Laboratory studies include a 24-hour urine study for creatinine clearance and total protein, full blood count, and chemistry and electrolyte profiles. Hepatitis B and C, human immunodeficiency virus (HIV) and cytomegalovirus (CMV) testing are done to assess for the presence of any transmissible diseases. An ECG and chest X-ray are also done. A renal ultrasound and a renal arteriogram or three-dimensional CT are performed to ensure that the blood vessels supplying each kidney are adequate and that there are no anomalies, and to determine which kidney will be removed.

A transplant psychologist or social worker will determine whether the individual is emotionally stable and able to deal with the issues related to organ donation. All donors must be informed about the risks and benefits of donation, the potential short-term and long-term complications, and what can be expected during the hospitalisation and recovery phases. Although the cost of the evaluation and surgery are covered by Medicare and/or private health insurance, there is no compensation available for lost wages during the post-hospitalisation recovery period, which can last 6 weeks or longer. The laparoscopic donor nephrectomy procedure is minimally invasive with fewer risks and shorter recovery time.⁶⁸

Paired donor exchange is a viable alternative when there is ABO incompatibility. Another option is to use plasmapheresis. In a limited number of transplant centres, plasmapheresis is used to remove antibodies from the recipient where there is an ABO incompatibility or a positive cross-match between the donor and recipient. (Cross-matching is discussed in Ch 13.) This allows transplant candidates to receive kidneys from live donors with blood types that have traditionally been considered incompatible. Following the transplant, the patient undergoes additional plasmapheresis treatments.

Deceased donors

Deceased (cadaver) kidney donors are either relatively healthy individuals who have suffered an irreversible brain injury (brain death) or people who have been withdrawn from life-sustaining treatment (cardiac death). The most common causes of donor death are cerebrovascular accident, cerebral trauma from motor vehicle accidents or gunshot wounds, intracerebral or subarachnoid haemorrhage and anoxic brain damage caused by cardiac arrest. Brain death is the irreversible cessation of brain function, although cardiovascular function is supported by a ventilator. Donation after cardiac death (DCD) has recently been re-introduced in Australia; donors are defined as patients who are certified dead using the criterion of irreversible cessation of circulation. As soon as cardiac death is confirmed, the retrieval procedure is commenced in order to minimise warm ischaemic time. Very few patients meet the DCD criteria to qualify as potential organ donors. The age range of most suitable cadaveric kidney donors is from 2 to 70 years. The age of the donor is less important than the quality of kidney function. The donor must be free of active IV drug abuse, severe hypertension, longstanding diabetes mellitus, malignancies, sepsis and communicable diseases, including HIV, hepatitis B and C, syphilis and tuberculosis. All states and territories of Australia, and New Zealand, have legislation for the removal of tissues (including organs) after death, for the purpose of transplantation.⁶⁹ Permission from the donor’s legal next-of-kin is routinely sought, even if the donor carried a signed donor card, although this is not a legal requirement.⁶⁵

Allocation of resources

CLINICAL PRACTICE

Situation

A transplant nurse coordinator is considering her feelings about two patients who are being evaluated for placement on the cadaveric kidney transplant waiting list. One patient is a 40-year-old Māori school teacher. She is married and has two children. The other patient is a 22-year-old unemployed Pakeha (European) male who is actively using cocaine. He misses three to four dialysis treatments per month and does not take his antihypertensive medications consistently. What do you feel about these two situations? How would you make a judgement?

Important points for consideration

• It is tempting to believe that nurses can be neutral, basing allocation of scarce resources on need rather than worth. However, it is sometimes difficult to withhold value judgements when caring for patients.

• Psychological, physiological and adherence factors are included in the assessment process for eligibility for organ transplantation.

• In kidney transplantation, the organ is transplanted into the patient who has received the most points based on a scoring system, regardless of the healthcare provider’s opinion of the patient’s worth. If a patient is denied transplant candidacy on this basis, they must be given a chance to change or improve the problem or condition in a specified period of time.

• The national organ allocation system is designed to be unbiased about the patient in all respects. Once a patient is placed on the list for transplantation, that patient is deemed of no greater or lesser worth than any other patient.

• Since organ donation is voluntary and altruistic in both New Zealand and Australia, any concerns that the system of procurement and transplantation is not fair may negatively affect the pool of available organs.

CRITICAL THINKING QUESTIONS

1. What does the Code of Conduct/Ethics of the Australian Nursing and Midwifery Council or the Nursing Council of New Zealand say about how nurses should view patients?

2. What are your feelings about which of these two patients should receive the next available organ? Why do you believe this?

The kidneys are removed and preserved. They can be preserved for up to 72 hours but most transplant surgeons prefer to transplant kidneys before the cold time (time outside of the body when being transported from the deceased donor to the recipient) reaches 24 hours. Experience has shown that prolonged cold time increases the likelihood that the kidney will not function immediately, and the transplant recipient will require dialysis until the ATN from the extended cold time resolves.

In Australia, cadaveric kidneys are distributed by the National Kidney Matching Scheme via the Red Cross Blood Bank using an objective computerised point system. A similar system exists in New Zealand. A balance is maintained between donor and recipient numbers across all states. When a donor becomes available, the donor’s HLA data, ABO type, age, antibody level and length of time waiting are entered into the national computer and compared with the data of all patients awaiting transplantation locally and nationwide. Points are given for how close the HLA match is, how long the patient has been waiting, whether the antibody level is unusually high and whether the recipient is less than 18 years old. Extra points are given for high antibody levels because this can severely limit the number of donors with whom the patient will not have a positive cross-match. One kidney is offered to the recipient with the most points in the same state as the donor. The other kidney may go interstate. If no patients in the state are suitable, the organ is offered to other states. When a kidney arrives at the recipient’s transplant centre, a final cross-match is done. The final cross-match must be negative for the cadaveric transplant to proceed. (Cross-matching is discussed in Ch 13.)

The only exception to the above plan is if a patient needs an urgent transplant or if a donor and recipient do not mismatch on any of the six HLA antigens (zero antigen mismatch). In these situations, the patient meeting either one of these criteria goes to the top of the list. Urgent transplants are given priority because the patient is facing imminent death if not transplanted (e.g. a patient who has no vascular access sites left and can no longer dialyse). Zero antigen mismatches are given priority because statistically these grafts have much better survival rates. If a zero antigen mismatch patient is identified nationally, one of the donor kidneys must be sent to that recipient’s transplant centre regardless of location.

SURGICAL PROCEDURE

Live donor

The donor nephrectomy is performed by a urologist or transplant surgeon. The donor’s surgery begins an hour or two before the recipient’s surgery is started. The recipient is surgically prepared for the kidney transplant in a nearby operating room. The use of a laparoscopic donor nephrectomy procedure is minimally invasive with fewer risks and shorter recovery time. This procedure is now being used as the primary method of live kidney procurement.⁶⁸ The laparoscopic approach significantly decreases the hospital stay, pain, operative blood loss, debilitation and length of time off work. For these reasons, the number of people willing to donate a kidney has increased significantly.

For a conventional nephrectomy, the donor is placed in the lateral decubitus position on the operating table so that the flank is presented laterally. An incision is made at the level of the eleventh rib. The rib may have to be removed to provide adequate visualisation of the kidney. After removal of the kidney, it is flushed with a chilled, sterile electrolyte solution and prepared for immediate transplant into the recipient. The nephrectomy takes about 3 hours. The short cold time is the primary reason for the success of living donor transplants.

Kidney transplant recipient

The transplanted kidney is usually placed extraperitoneally in the iliac fossa. The right iliac fossa is preferred to facilitate anastomoses and minimise the occurrence of ileus.

Before any incisions are made, a urinary catheter is placed into the bladder. An antibiotic solution is instilled to distend the bladder and decrease the risk of infection. A crescent-shaped incision is made extending from the iliac crest to the symphysis pubis. The peritoneum is left intact (see Fig 46-19).

Figure 46-19 A, Surgical incision for a renal transplant. B, Surgical placement of transplanted kidney.

Rapid revascularisation is critical to prevent ischaemic injury to the kidney. The donor artery is anastomosed to the recipient’s internal iliac (hypogastric) or external iliac artery. The donor vein is anastomosed to the recipient’s external iliac vein. Kidney transplants with living donors can be technically more difficult because the blood vessel lengths can be shorter than in cadaveric transplants.

When the anastomoses are complete, the clamps are released and blood flow to the kidney is re-established. The kidney should become firm and pink. Urine may begin to flow from the ureter immediately. Mannitol or frusemide may be administered to promote diuresis.

The donor ureter in most cases is then tunnelled through the bladder submucosa before entering the bladder cavity and being sutured in place. This approach is called ureteroneocystostomy. This allows the bladder wall to compress the ureter as it contracts for micturition, thereby preventing reflux of urine up the ureter into the transplanted kidney. The transplant surgery takes approximately 3–4 hours.

NURSING MANAGEMENT: KIDNEY TRANSPLANT RECIPIENT

The successful recovery and rehabilitation of the recipient are made possible with careful nursing assessment, diagnosis, intervention and evaluation of all body systems. With a hospital length of stay averaging 4–5 days, discharge planning and teaching needs must be identified and addressed early in the hospital course.

Preoperative care

Nursing care of the patient in the preoperative phase includes emotional and physical preparation for surgery.⁷⁰ Because the patient and family may have been waiting years for the kidney transplant, a review of the operative procedure and what can be expected in the immediate postoperative recovery period is necessary. It is important to stress that there is a chance the kidney may not function immediately and that dialysis may be required for days to weeks. The need for immunosuppressive drugs and measures to prevent infection must be reviewed.

To ensure the patient is in optimal physical condition for surgery, an ECG, chest X-ray and laboratory studies are ordered. Dialysis may be required before surgery for any significant abnormality such as fluid overload or hyperkalaemia. A patient on PD must empty the peritoneal cavity of all dialysate solution before going to surgery. Because dialysis may be required after transplantation, the patency of the vascular access must be maintained. The vascular access extremity should be labelled ‘dialysis access, no procedures’ to prevent use of the affected extremity for blood pressure measurement, blood drawing or IV infusions.

Postoperative care

Live donor

The usual postoperative care for the donor is similar to that following conventional or laparoscopic nephrectomy (see Ch 45). Close monitoring of renal function to assess for impairment and of the haematocrit to assess for bleeding is essential. The serum creatinine level should be less than 120 mmol/L and the haematocrit should not fall more than 3–6 points. The pain that a donor who has had a conventional nephrectomy experiences is greater than that of the donor who has had a laparoscopic procedure. Generally, all donors have more pain than their recipients. Conventional donors are ready to be discharged from the hospital in 4–7 days and can usually return to work in 6–8 weeks. Laparoscopic donors are able to be discharged from the hospital in 2–4 days and can return to work in 4–6 weeks. The donor is generally seen by the surgeon 1–2 weeks after discharge.

Nurses caring for the living donor need to acknowledge the precious gift that this person has given. The donor has taken physical, emotional and financial risks to assist the recipient. It is vital that they are not forgotten postoperatively. The donor will need even greater support if the donated organ does not work immediately or for some reason fails.

Recipient

The first priority during this period is maintenance of fluid and electrolyte balance. In many centres, kidney transplant recipients are admitted to specialised kidney transplant units because of the close monitoring required.⁷¹ Very large volumes of urine may be produced soon after the blood supply to the transplanted kidney is re-established. This diuresis is due to: (1) the new kidney’s ability to filter urea, which acts as an osmotic diuretic; (2) the abundance of fluids administered during the operation; and (3) initial renal tubular dysfunction, which inhibits the kidney from concentrating urine normally. Urine output during this phase may be as high as 1 L per hour and gradually decreases as the serum urea and creatinine levels return towards normal. Urine output is replaced mL for mL hourly for the first 12–24 hours. Central venous pressure readings are essential for monitoring postoperative fluid status. Dehydration must be avoided to prevent subsequent renal hypoperfusion and renal tubular damage. Electrolyte monitoring to assess for the hyponatraemia and hypokalaemia often associated with rapid diuresis is critical. Treatment with potassium supplements or 0.9% normal saline solution infusion may be indicated. IV sodium bicarbonate may also be required if the patient becomes acidotic.

ATN can occur because of prolonged cold ischaemic times and the use of marginal donors. The ischaemic damage from extended cold times causes ATN. While the patient has ATN, dialysis is required to maintain fluid and electrolyte balance. Some patients have high-output ATN with the ability to excrete fluid but not metabolic wastes or electrolytes. Other patients have oliguric or anuric ATN. These patients are at risk of fluid overload in the immediate postoperative period and must be assessed closely for the need for dialysis. The period of ATN can last anywhere from days to weeks, with gradually improving kidney function. Most patients with ATN will be discharged from the hospital on dialysis. This is extremely discouraging for the patient, who will need reassurance that renal function usually improves. Dialysis will be discontinued when urine output increases and serum creatinine and urea levels begin to normalise.

A sudden decrease in urine output in the early postoperative period is a cause for concern. It may be due to dehydration, rejection, a urine leak or obstruction. A common cause of early obstruction is a blood clot in the urinary catheter. Catheter patency must be maintained as the catheter remains in the bladder for 3–5 days to allow the bladder anastomosis to heal. If blood clots are suspected, gentle catheter irrigation with an order from the healthcare provider can re-establish patency.

Postoperative teaching should include the prevention and treatment of rejection, infection and complications of surgery, and the purpose and side effects of immunosuppression. Patients should be aware that rejection is a common occurrence during the first 3 months after transplant. Frequent blood tests and clinic visits help detect rejection early. Patient education to ensure a smooth transition from hospital to home is an integral part of the nursing care.⁷¹

IMMUNOSUPPRESSIVE THERAPY

The goal of immunosuppression is to suppress the immune response adequately to prevent rejection of the transplanted kidney while maintaining sufficient immunity to prevent overwhelming infection. Immunosuppressive therapy is discussed in Chapter 13.

COMPLICATIONS OF TRANSPLANTATION

Complications of KRT, including PD, HD and kidney transplantation, are compared in Table 46-12.

TABLE 46-12 Complications of kidney replacement therapy

Rejection

Rejection is one of the major problems following kidney transplantation.^22,⁷² Rejection can be hyperacute, acute or chronic. These types of rejection are discussed in Chapter 13. Patients with chronic rejection should be put on the transplant list in the hope that they can be retransplanted before dialysis is required.

Infection

Infection remains a significant cause of morbidity and mortality after transplantation.^22,⁷² The transplant recipient is at risk of infection because of suppression of the body’s normal defence mechanisms by surgery, immunosuppressive drugs and the effects of ESKD. Underlying systemic illness, such as diabetes mellitus or systemic lupus erythematosus, malnutrition and older age can further compound the negative effects on the immune response. At times the signs and symptoms of infection can be subtle. Nurses caring for transplant recipients must be astute in their observations and assessment because prompt diagnosis and treatment of infections will improve patient outcomes.

The most common infections observed in the first month after transplantation are similar to those acquired by any postoperative patient, such as pneumonia, wound infections, IV line and drain infections, and urinary tract infections. Fungal and viral infections are common because of the patient’s immunosuppressed state. Fungal infections can include Candida, Cryptococcus, Aspergillus and Pneumocystis carinii pneumonia (PCP; also known as Pneumocystis jirovecii). Fungal infections are difficult to treat, require prolonged treatment periods and often involve the administration of nephrotoxic drugs. Transplant recipients usually receive prophylactic antifungal drugs to prevent these infections, such as nystatin, fluconazole and sulfamethoxazole-trimethoprim.

Viral infections including CMV, Epstein-Barr virus, herpes simplex virus, varicella-zoster virus and polyomavirus (e.g. BK virus) can be primary or a reactivation of existing disease. Primary infections occur as new infections after transplantation from an exogenous source, such as the donated organ or blood transfusion. Reactivation occurs when a virus exists in a patient and becomes reactivated after transplantation because of immunosuppression.

CMV is one of the most common viral infections. If a recipient has never had CMV and receives an organ from a donor with a history of CMV, antiviral prophylaxis will be administered (e.g. ganciclovir, valaciclovir). If a primary active CMV infection is diagnosed or there is symptomatic reactivation of CMV, IV ganciclovir will be given. Other antiviral drugs, such as aciclovir, can also be used to treat systemic viral infections.

Cardiovascular disease

Transplant recipients have an increased incidence of atherosclerotic vascular disease. Cardiovascular disease is the leading cause of death after kidney transplantation.²² Hypertension, hyperlipidaemia, diabetes mellitus, smoking, rejection, infections and increased homocysteine levels can all contribute to cardiovascular disease. Immunosuppressants can worsen hypertension and hyperlipidaemia. It is important that the patient be taught to control risk factors such as elevated cholesterol, triglyceride and blood glucose levels and weight gain. Adherence to the prescribed antihypertensive regimen is essential not only to prevent cardiovascular events but also to prevent damage to the new kidney. (Hypertension is discussed in Ch 32.)

Withdrawing treatment

CLINICAL PRACTICE

Situation

A 70-year-old patient with diabetes mellitus and chronic kidney disease who has been on dialysis for 10 years tells the nurse he wants to discontinue his dialysis. His quality of life has diminished during the past 2 years since his wife died. He is not a prospective transplant patient.

Important points for consideration

• Quality of life is an important consideration for patients when weighing whether to begin or discontinue treatment.

• Quality-of-life decisions often weigh the benefit against the burden of treatment. When a treatment becomes too burdensome, the patient (if competent) may request to withdraw the treatment.

• A determination must be made whether there is some other treatable problem, such as depression, that may be clouding the patient’s judgement.

• Patient autonomy—the patient’s right to self-determination regarding treatment decisions—applies to both initiating and discontinuing treatment.

• Assessing a patient’s capacity to make healthcare decisions, especially related to end-of-life issues, is a complex process involving physical, psychological, social, spiritual and quality-of-life factors.

• If a decision is made to withdraw treatment, the healthcare team, patient and family should develop an appropriate follow-up plan that includes palliative care and hospice support.

CRITICAL THINKING QUESTIONS

1. How should the nurse respond to the patient’s request?

2. What is the position of the Australian Nursing and Midwifery Council or the Nursing Council of New Zealand on withdrawing or withholding treatment that no longer benefits the patient or causes suffering?

Malignancies

The overall incidence of malignancies in kidney transplant recipients is about 100 times greater than in the general population.²² The primary cause of this increased incidence is the immunosuppressive therapy. Not only do immunosuppressants suppress the immune system but they also suppress the ability to fight infection and the production of abnormal cells such as cancer cells. The malignancies include cancer of the skin, lips, kidney, hepatobiliary system, vulva and perineum, lymphomas, Kaposi’s sarcoma and other sarcomas. In Australia it is thought that up to 30% of patients will develop skin cancer within 10 years following a kidney transplant.²² The patient must be taught the importance of avoiding sun exposure by using protective clothing and sunscreens to minimise the incidence of skin cancers. Regular screening for cancer is also an important part of the transplant recipient’s preventative care.

Recurrence of the original kidney disease

Recurrence of the original disease that destroyed the native kidneys occurs in some kidney transplant recipients.²² It is most common with certain types of glomerulonephritis, IgA nephropathy, diabetes mellitus and focal segmental sclerosis. Disease recurrence can result in the loss of a functioning kidney transplant. Patients must be advised before transplant whether they have a disease known to recur. For patients with type 1 diabetes mellitus, simultaneous kidney and pancreas transplants may help to avoid disease recurrence.

Corticosteroid-related complications

Aseptic necrosis of the hips, knees and other joints can result from chronic corticosteroid therapy and CKD-MBD. Other significant problems related to corticosteroids include peptic ulcer disease, glucose intolerance and diabetes, cataracts, hyperlipidaemia, and an increased incidence of infections and malignancies. In the first year after transplantation, corticosteroid doses are usually decreased to 5–10 mg a day. The use of tacrolimus and cyclosporin has allowed corticosteroid doses to be much lower than they were in the past. Some patients have been withdrawn successfully from corticosteroids 1.5–2 years after transplantation, thus eliminating these problems. Vigilant monitoring for side effects of corticosteroids and early treatment is essential.

Gerontological considerations: chronic kidney disease

The incidence of ESKD in Australia and New Zealand is increasing most rapidly in older patients. The mean age of the ESKD population has increased to 59.5 years in Australia and 57.5 years in New Zealand. Recent data indicate that of all patients who have ESKD, about 45% are 65 years or older.²² The most common diseases leading to CKD in the older adult are diabetes mellitus and hypertension. Medicare expenditure is expected to increase as the ESKD population ages and so suffers from a greater number of coexisting conditions.

The care of this older population is particularly challenging, not only because of the normal physiological changes of ageing that occur, but also because of the disabilities, chronic diseases and number of comorbid conditions that develop.⁷³ Physiological changes of clinical importance in older CKD patients include diminished cardiopulmonary function, bone loss, immunodeficiency, altered protein synthesis, impaired cognition and altered drug metabolism.⁷³ Malnutrition is common in older ESKD patients for a variety of reasons, including lack of mobility, lack of understanding of basic nutritional requirements, social isolation, physical disability, impaired cognitive function and malabsorption problems.

When conservative therapy for CKD is no longer effective, older patients need to consider what is the best treatment modality based on their health, personal preferences and support available. PD allows the patient to be more mobile and to enjoy an increased sense of control over the illness. PD causes less haemodynamic instability than HD, but it does require self-care or assistance from another person.

Many patients 65 years of age and older select treatment with HD because of a lack of assistance in the home and a reluctance to manage the technology of dialysis. Establishing vascular access for HD may be somewhat of a concern for older patients because of atherosclerotic changes. Although transplantation is an option, elderly patients must be carefully screened to ensure that the benefits outweigh the risks. A living donor is preferable so that there is not a prolonged waiting time.

The most common cause of death in elderly CKD patients is cardiovascular disease (MI, stroke), followed by withdrawal from dialysis. If a competent patient decides to withdraw from dialysis, it is essential to support the patient and family.⁷³ Ethical issues to be considered in this situation include patient competency, benefit versus burden of treatment, and the futility of treatment (see the Clinical practice box). Withdrawal from treatment is not a failure if the patient is well informed and comfortable with the decision.

The increasing number of elderly, debilitated ESKD patients receiving dialysis has raised a number of ethical concerns about the use of scarce resources in a population with a limited life expectancy. Substantial evidence exists showing the success of dialysis (especially PD) in the elderly. Quality of life has also been reported to be good to excellent in many older ESKD patients receiving dialysis. There appears to be no justification for excluding older adults from dialysis programs. Rationing dialysis on the basis of age alone is not supported based on current outcome and quality-of-life data.

The patient with chronic kidney disease

CASE STUDY