acute tubular necrosis (ATN).Nephrology is the medical specialty that manages diseases of the kidney and renal replacement therapy (RRT; e.g. dialysis and transplant). While only larger hospitals will have a renal unit, most will have a visiting nephrologist, and all hospitals will have inpatients with renal impairment. The principles of fluid balance and managing a patient with renal failure are vital skills for every clinician.
• Acute kidney injury (AKI): a common reason for emergency admission and it also frequently develops in hospital. The commonest cause is ‘pre-renal’ haemodynamic disturbance such as dehydration, sepsis, or hypotension combined with drugs including NSAIDs, ACEIs, and diuretics. It is often multifactorial.
• Nephrotic syndrome: caused by a number of glomerular diseases and is generally managed in the outpatient clinic. However, some are admitted for renal biopsy/fluid management.
• Chronic kidney disease (CKD): managed in the community and clinic. However, patients admitted for unrelated problems are at risk of further renal deterioration (acute-on-chronic failure).
• Haemodialysis: patients attend the hospital three times weekly for life-sustaining treatment. Hospital admissions are common, e.g. with complications of dialysis access or comorbidity such as ischaemic heart disease.
• Renal transplant: a subspecialty field encompassing both surgery and medicine that you will only find at larger teaching hospitals. Most renal units will care for transplant patients after the first few months.
Usually done as a day-case procedure under US guidance.
Either an emergency/temporary dialysis line (vascath or tunnelled catheter) or for patients nearing end-stage renal failure elective arteriovenous fistula.
Usually done by an interventional radiologist to relieve upper urinary tract obstruction, especially where there is intercurrent infection.
Renal transplant or donor nephrectomy if based in specialist/teaching hospital.
Practise fluid balance assessments, learn about intrinsic renal disease, and speak to a dialysis patient to understand the restrictions they face (e.g. dietary, fluid, lifestyle, and psychosocial). See Table 21.1 for recent studies.
Occurs in response to renal hypoperfusion, e.g. in dehydration, hypotension, and sepsis (or more rarely in heart failure or renal artery stenosis). Urine is appropriately concentrated to retain water and salt. Serum urea is often elevated proportionately more than creatinine. Usually responds to treatment of underlying cause. Uncorrected pre-renal failure acute tubular necrosis (ATN).
Usually ATN following pre-renal insults. Often results in established renal failure despite fluid replacement and BP support. May require temporary haemodialysis. Also includes intrinsic renal disease such as glomerulonephritis and interstitial nephritis.
Secondary to blocked urinary drainage. Lower urinary tract obstruction often due to prostate disease urinary retention. Upper tract obstruction may be caused by stones, intrinsic (e.g. urothelial tumour) or extrinsic (metastases) compression.
To diagnose dehydration as cause of renal failure or fluid overload due to reduced urine output. Cannot be done over the phone! Aim for euvolaemia rather than a given urine output in patients with established renal impairment.
Blood or protein in the urine is suggestive of glomerular disease. Leucocytes (pyuria) and nitrites are seen on a urine dipstick in UTI which is confirmed by MC&S.
US to exclude urinary tract obstruction and assess size of kidneys and cortical thickness. Also diagnoses structural kidney disease (e.g. autosomal dominant polycystic kidney disease (ADPKD)). CT of kidneys/ureters/bladder gives more detailed information about entire urinary tract and identifies renal calculi.
Often forgotten but it is vital to identify agents that may have contributed to or compounded renal failure (ACEI, NSAIDs, diuretics). Drugs that are renally excreted must be given in reduced doses in renal failure to prevent accumulation toxicity (e.g. some opiates and antibiotics).
Renal haemodynamics: the key to understanding most cases of AKI
The kidney filters about 200 L of blood per day. This function is expressed as the glomerular filtration rate (GFR; mL/min/1.73 m2). This can be measured indirectly by nuclear medicine renography or can be estimated based on serum creatinine/cystatin C and sex/age/weight.
GFR is maintained across a wide range of systemic blood pressure and changes in circulating volume by renal autoregulation; vasoconstriction of the efferent arteriole maintains hydrostatic pressure within the glomerulus at times of low blood pressure. Afferent arteriolar tone protects the glomerular vessels from high systemic blood pressure.
Sepsis and drugs (e.g. ACE inhibitors and NSAIDs) interfere with these mechanisms and cause renal failure especially in the context of dehydration or hypotension. Initially this will cause prerenal failure but it will progress to ATN if not corrected in time.
Table 21.1 Recent studies in nephrology
| Details | Trial | Comments |
| 2002 JAMA N = 1094 | African American Study of Kidney Disease and Hypertension (AASK) | No difference in CKD progression among African American patients with either intensive vs conservative BP control |
| 2006 NEJM N = 1432 | Correction of Hb and Outcomes in Renal Insufficiency (CHOIR) | Erythropoietin therapy targeting a higher Hb level of 13.5 g/dL (vs 11.3), higher mortality risk + hospitalizations for congestive heart failure in patients with non-dialysis CKD + anaemia |
| 2007 NEJM N = 1645 | Efficacy Limiting Toxicity Elimination-Symphony trial (ELITE-Symphony) | Immunosuppression with tacrolimus in renal transplantation higher estimated glomerular filtration rate, graft survival, and lower rates of rejection at 12 months (compared to 3 other regimens) |
| 2010 NEJM N = 828 | The Initiating Dialysis Early and Late (IDEAL) | No difference in survival/clinical outcomes between early vs late initiation of dialysis in CKD (stage V) |
| 2016 NEJM N = 620 | Artificial Kidney Initiation in Kidney Injury (AKIKI) | No mortality difference between early or delayed RRT in ICU patients with AKI |
You should be aware of the life-threatening complications of renal failure requiring emergency haemodialysis.
Patients with reduced or no urine output will become fluid overloaded. A trial of high-dose diuretic is reasonable if the patient has some residual renal function but if they are anuric or a chronic haemodialysis patient they need immediate dialysis to remove excess fluid.
Dyspnoea, hypoxia, fine bibasal crackles, and CXR showing ‘bat’s wing’ appearance, alveolar shadowing.
Mild (5.5–6.0), moderate (6.1–6.9), severe (>7.0 mmol/L). Serum K+ >6.5 requires immediate attention. Features: weakness/cramps, paraesthesiae, hypotonia, focal neurological deficits and cardiac arrest.
ECG changes (a common exam question):
• Sinusoidal (‘sine wave’ pattern) QRST.
• Atrioventricular dissociation.
• 12-lead ECG (can be normal) and cardiac monitor.
• 10 mL of 10% calcium chloride IV (stabilizes the myocardium).
• Insulin (10 units soluble insulin)/glucose (50 mL of 50%) infusion (drives K+ into the cells).
• Nebulized salbutamol 10–20 mg.
• Enteral calcium polystyrene sulfonate can be given but takes hours to take effect.
• Consider dialysis if severe or refractory.
Systemic complications from accumulation of uraemic compounds (not urea per se). Neurological features include myoclonus and fluctuating GCS score. Can also cause haemorrhagic pericarditis. Initial dialysis should be short and slow to avoid disequilibrium syndrome. Gastric protection (e.g. PPI) may reduce risk of GI bleeds. Symptoms/signs: twitching, drowsiness, pericarditic chest pain with widespread ST changes on ECG and effusion on echocardiography.
Usually normal anion gap. Exclude other causes (e.g. DKA and lactic acidosis). Difficult to correct high K+ in presence of acidosis.
Kussmaul breathing, low pH, low HCO3−.
Uncommonly, dialysis is used to remove poisons/toxins (e.g. ethylene glycol and salicylates) even in patients with normal renal function.
Discussion with the boss
Intermittent haemodialysis vs continuous renal replacement therapy?
Typically 3–4-hour sessions, quickly corrects high K+ or high urea, can ultrafiltrate about >1 L fluid/hour using dialysis line or arteriovenous fistula. Not suitable for haemodynamically unstable patients or those with multiorgan failure.
(E.g. haemofiltration): lower efficiency but causes less haemodynamic instability. Takes place continually over 24–48 hours. Used in critical care setting and where patient requires inotrope/vasopressor support. May improve inflammatory milieu in sepsis.
There is no clear survival benefit of either technique. Consider on an individual patient basis (vital signs, comorbidities, other organ involvement, vascular access, availability of resources, etc.).
Deal with any life-threatening complication (high K+, pulmonary oedema, etc.).
• Baseline renal function if known (acute vs chronic).
• Previous renal failure or relevant renal history.
• Recent dehydrating illness or symptoms of fluid overload.
• Urinary problems such as prostatism, reduced output or UTI.
• Symptoms in keeping with multisystem disorder (e.g. weight loss, fever, joint pain, rash, ear or nose discharge, haemoptysis).
• Cardiovascular comorbidities especially PVD, hypertension, or heart failure.
• Diabetes (micro- or macrovascular complications?).
• Medications, especially ACEIs, ARB, diuretics, antibiotics, PPIs. Over-the-counter drugs including NSAIDs or herbal remedies.
• Family history (e.g. ADPKD, Alport’s syndrome).
• Intravascular: HR, BP (postural), capillary refill, JVP, urine output (NB urine output is not a useful indicator of fluid status in established renal failure).
• Extravascular: peripheral/pulmonary oedema, ascites, weight.
• Stigmata of systemic disease (joints/lungs/skin/chest/eyes).
• Exclude urinary retention/BPH.
• Exclude uraemic complications (e.g. pericarditis/encephalopathy).
• Peripheral pulses (PVD and renal artery stenosis coexist) and arterial bruits.
• Urinalysis for protein/blood.
Imaging: to exclude urinary tract obstruction and to assess renal symmetry (renal artery stenosis or congenital shrunken kidney), cortical thickness (reduced in CKD) and scarring (e.g. in reflux nephropathy).
Correct fluid imbalance: IV fluids where dehydrated, diuretics/fluid restriction/ultrafiltration where overloaded.
Medication review: stop any drugs which may contribute to renal failure or cause toxicity.
Dietary advice: low K+ or PO43− diet may be appropriate. Variable fluid restriction where oliguric/anuric.
• Urine albumin:creatinine ratio (ACR) to quantify proteinuria.
• Autoimmune panel to exclude vasculitis.
• Myeloma screen (serum and urine electrophoresis, immunoglobulins).
• Renal biopsy if suspicion of intrinsic renal disease (other than ATN) or diagnosis/prognosis unclear.
• Septic screen where appropriate.
• Bone profile, PTH, and haematinics (iron studies, vitamin B12, and folate) to manage complications of renal failure.
• Call GP or other hospital to establish baseline renal function.
• Other renal imaging (e.g. CT kidneys, ureters, and bladder (KUB) for stones, renal angiogram for renal artery stenosis).
Discussion of management options: such as modes of RRT, or conservative management if patient unlikely to benefit from RRT. Immunosuppression if immune-mediated renal disease.
Vascular access: avoid cannulae and phlebotomy in forearm veins, which may later be needed for arteriovenous fistula!
See Table 21.2 for definition.
Table 21.2 AKI defined using RIFLE criteria
| GFR | U/O | |
| Risk |
1.5 × Cr
25%  GFR |
<0.5 mL/kg/hour (6 hours) |
| Injury |
2 × Cr
50% GFR |
<0.5 mL/kg/hour (12 hours) |
| Failure |
3 × Cr
75% GFR |
<0.3 mL/kg/hour (2 hours) Anuria (12 hours) |
| Loss | No renal recovery after 4 weeks | |
| End-stage failure | No renal recovery after 12 weeks | |
Cr, creatinine; GFR, glomerular filtration rate; RIFLE, Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease; U/O, urine output.
• 2% of all hospital inpatients, 40% on admission to critical care.
• Community AKI particularly in elderly, ACEIs/ARBs, prostate disease.
• Assume all renal failure is acute until proven otherwise (historical bloods, shrunken kidneys).
Commonly ATN in response to ischaemic insult. Mechanisms include acute inflammation in response to sterile tubular cell injury and intrarenal vasoconstriction. AKI has deleterious effects on other organ systems (organ ‘cross-talk’).
See Fig. 21.1.
• Obstruction (stones, BPH, catheter).
• Antibiotics (e.g. gentamicin, penicillins).
• Tubular (ischaemia, myeloma, rhabdomyolysis, contrast).
• Assess volume status (pulse, BP, peripheral perfusion, JVP).
• Check urine dipstick for evidence of renal damage (blood + protein).
• PO/IV rehydration if hypovolaemic.
• Relieve any obstruction (US scan renal tract can help diagnosis).
• Treat any associated hyperkalaemia.
• Adjust doses of other medication in relation to renal function.
• Monitor creatinine regularly.
A renal biopsy indicated where a specific treatment (e.g. immunosuppression) is available or where renal prognosis is important to guide further management.
• 40–50% mortality in critical care patient requiring RRT.
• 5% mortality if single organ failure.
• 70–80% renal recovery (age and comorbidities as determinants).
• Worse outcomes in oliguric/fluid overloaded patients.
Honours
Recommendations:
• Earlier recognition of AKI that develops in hospital.
• Involvement of senior and specialist staff early on.
• 24-hour access to renal US and nephrostomy service.
• Prompt recognition of the sick patient and critical care referral.
• Renal biochemistry and urinalysis for all emergency admissions.
Fig. 21.1 Causes of reduced urine output. AAA, abdominal aortic aneurysm; IBD, inflammatory bowel disease; TB, tuberculosis. Reproduced with permission from Piers Page and Greg Skinner, Emergencies in Clinical Medicine, 2008, Oxford University Press.
This renal emergency is caused by immunologically mediated disease the following:
• Rapid deterioration in renal function.
• ‘Crescents’: inflammatory infiltrate within Bowman’s capsule which can compress and destroy glomerulus.
• Blood/protein in urine (beware anuria).
• Often extrarenal features (e.g. pulmonary haemorrhage, rash, and joint pain).
• Pulmonary haemorrhage is life-threatening and requires aggressive management.
May respond to immunotherapy so early recognition, biopsy, and treatment are a priority.
Pauci-immune (60%): usually antineutrophil cytoplasmic antibody-associated small vessel vasculitis; microscopic polyangiitis (MPA) or granulomatosis with polyangiitis (GPA, previously known as Wegener’s granulomatosis).
Immune-complex mediated (20%): Worldwide post-infectious glomerulonephritis is a common cause but lupus nephritis and Henoch–Schönlein purpura/IgA nephropathy are more common in the West.
Anti-GBM disease (Goodpasture’s disease) (15%): caused by IgG autoantibodies to alpha-3 (IV) chain of collagen found in glomerular (and alveolar) basement membrane.
Specific treatments:
• Pulsed methylprednisolone and high-dose oral steroids.
• Alkylating agent such as cyclophosphamide followed by azathioprine or mycophenolate mofetil.
• Plasma exchange (where severe renal failure at presentation or pulmonary haemorrhage).
Urine and blood test abnormalities (haematology, biochemistry, and immunology) in renal failure are highlighted in Table 21.3.
Table 21.3 Abnormalities in renal failure
| Parameter | Normal range | Renal failure |
| Biochemistry | ||
| Urea (U) | 3–7 |  (esp. pre-renal) |
| Creatinine (Cr) | 80–120 | (esp. rhabdomyolysis) |
| Sodium (Na+) | 135–145 | (dehydration) dilution/urinary loss |
| Potassium (K+) | 3.5–5 | in impaired excretion |
| Bicarbonate (HCO3−) | 18–25 | in renal wasting/ H+ excretion |
| Calcium (Ca2+) | Corr 2.1–2.3 | in impaired absorption/ vitamin D |
| Phosphate (PO43−) | 0.8–1.2 | in reduced urinary excretion |
| Parathyroid hormone (PTH) | 25–75 | in renal failure |
| Serum electrophoresis | Monoclonal band in myeloma | |
| Immunoglobulins (Ig) |
Immunoparesis in myeloma Ig M/G in infection Ig A in IgA nephropathy |
|
| Creatine kinase (CK) | 25–200 | in rhabdomyolysis |
| Haematology | ||
| Haemoglobin (Hb) | 11.5–15 | Renal anaemia ( EPO secretion) |
| Platelets (Pl) | 150–400 | in thrombotic microangiopathy |
| Ferritin | >20 | in iron deficiency |
| Transferrin saturation | 20% | Functional iron deficiency |
| Vitamin B12/ folate | Exclude other causes of anaemia | |
| Immunology | ||
| ANCA | Autoimmune vasculitis | |
| ANA/anti dsDNA | SLE | |
| C3/C4 | in lupus, SBE, cholesterol emboli |
|
| Anti-GBM | Goodpasture’s disease | |
| Urine | ||
| Albumin:creatinine | >2.5 | Quantify proteinuria |
| Microscopy | Crystals, red cell casts | |
| Bence Jones protein | Immunoglobulin light chain | |
| 24-hour collection | Investigate stone | |
Patients may notice swollen ankles or frothy urine.
• Focal segmental glomerulosclerosis (FSGS)
• Minimal change disease (MCD)
FSGS, MCD, and MN can be primary/‘idiopathic’ or secondary (drugs, infection).
• Immobility/debility from oedema and skin breakdown.
• Infection (immunoglobulins lost in urine, complication of treatment).
• Thromboses (usually venous, arterial seen in antiphospholipid syndrome).
• Optimize BP, cholesterol, and proteinuria (ACEI).
• Infection prophylaxis (vaccines, co-trimoxazole, etc.).
• Anticoagulation if serum albumin <20.
• Primary FSGS/MCD: steroids and/or calcineurin inhibitor (e.g. tacrolimus).
• Idiopathic MN: one-third remit spontaneously but one-third progressive. 6 months of conservative management followed by high-dose steroids/alkylating agent if evidence of progression. Recently found to be caused by anti-PLA2R antibodies.
• Amyloid: cytotoxic myeloablative therapy to deplete pathogenic plasma cells.
• Diabetes: optimize HbA1c, BP, and ACEI.
Proteinuria: why all the fuss?
• Albuminuria is a sensitive sign of renal disease.
• Proteinuria in itself is a risk factor for progression of CKD, hence indications for ACEI/strict BP control.
• Microalbuminuria in the general population is predictive of cardiovascular morbidity and mortality.
Most labs now do ACR on a spot urine sample. 24-hour collections are inconvenient and rarely required.
See Table 21.4.
Table 21.4 Classification and biochemical findings in CKD (according to NICE CKD guidelines 2014)
| GFR and ACR categories and risk of adverse outcomes | Urine ACR (mg/mmol) | ||||
| <3 | 3–30 | >30 | |||
| A1 | A2 | A3 | |||
| GFR categories (mL/min/1.73 m2), description and range | ≥90 Normal and high | G1 | No CKD unless other markers of kidney damage | Moderately risk |
High risk |
| 60–89 Mild reduction | G2 | Moderately risk |
High risk | ||
| 45–59 Mild–moderate reduction | G3a | Moderately risk |
High risk | Very high risk | |
| 30–44 Moderate reduction | G3b | High risk | Very high risk | Very high risk | |
| 15–29 Severe reduction | G4 | Very high risk | Very high risk | Very high risk | |
| <15 Kidney failure | G5 | Very high risk | Very high risk | Very high risk | |
• CAKUT (congenital abnormalities of kidney and urinary tract).
• Inherited disorders, e.g. Alport’s syndrome, cystinosis.
• Other (e.g. tubulointerstitial nephritis).
• Often unknown (‘small kidneys’).
Presenting symptoms: usually discovered incidentally or on screening.
Often deduced from comorbidities such as diabetes with microvascular complications, cardiovascular disease, smoking, or known urological disease. Biopsy indicated where diagnosis unclear and result will change management.
NICE guidelines <140/90 or <130/80 mmHg if diabetic or urine ACR >70.
With ACEI/ARB if ACR >3 and diabetic, or >30 and hypertension, >70 with neither.
Statin and antiplatelet.
Occurs in response to phosphate retention and impaired hydroxylation of cholecalciferol. Treat with vitamin D analogue (alfacalcidol or calcitriol).
Dietary advice or phosphate binders for PO43−<1.5 mmol/L.
Consider iron supplements and erythropoietin aiming for Hb 10–12 g/dL.
Diuretics or fluid restriction if overloaded, encourage fluid intake if myeloma or polyuria (e.g. lithium).
Education, counselling and provision of arteriovenous fistula or peritoneal dialysis catheter where required.
Evaluate for renal transplantation (live donor where appropriate) in those likely to benefit.
ACEIs: hero or villain? Hero—where used appropriately!
• ACEIs preserve remaining GFR and reduce proteinuria through physiological fall in GFR via efferent arteriolar vasodilatation. Hence <25% fall in GFR or <30% rise in creatinine acceptable/expected.
• If greater change than this, consider renal artery stenosis/dehydration and stop/reduce.
Is caused by a malignant clone of plasma cells, which produce either immunoglobulins (usually IgG) or light chains. These infiltrate bone marrow (causing bone marrow failure) and cause lytic bone lesions throughout the skeleton.
Renal failure at presentation is common and affects up to one-half of all patients during the course of the disease. Renal function is an important prognostic factor in myeloma.
• Cast nephropathy or ‘myeloma kidney’: light chains which are filtered at the glomerulus bind to Tamm–Horsfall proteins in the tubular lumen forming casts. These obstruct urinary flow and cause ATN. A reactive tubulointerstitial infiltrate is also seen. Myeloma kidney is diagnosed on renal biopsy (check for normal platelets first).
• Hypercalcaemia from skeletal involvement causes polyuria and dehydration. Remember that serum calcium is usually low in AKI so the combination of AKI and hypercalcaemia should prompt myeloma investigations. All patients with myeloma (except those who are anuric) should be encouraged to drink at least 3 L/day.
• Infections: myeloma patients often have immunoparesis with low immunoglobulin levels predisposing them to infections. Sepsis with a disproportionate degree of AKI is commonly seen in myeloma and all such patients should have a complete septic screen.
• Treatment: most myeloma treatments are not nephrotoxic. However, patients may use over-the-counter NSAIDs, especially to treat bone pain.
• Less common: AL amyloidosis or light chain deposition disease.
Investigations: bone profile, immunoglobulins, serum and urine electrophoresis, serum free light chains for disease monitoring, renal biopsy where indicated.
1. Aggressive rehydration, particularly where hypercalcaemia present.
2. IV bisphosphonate if hypercalcaemia persists despite rehydration.
3. Prompt treatment of infections.
4. Treat anaemia (transfusion or erythropoietin).
5. Renal biopsy usually undertaken at presentation.
6. Definitive myeloma treatment regimens such as cyclophosphamide/dexamethasone/thalidomide or newer agents such as the proteasome inhibitor bortezomib will reduce the production of paraprotein/light chain.
7. Light chain removal treatment: there is evidence that extended dialysis sessions using high cut-off membranes (which remove higher-molecular-weight molecules than conventional ones) can reverse AKI in myeloma kidney. This should be done in conjunction with definitive therapy as listed above.
Is caused by skeletal muscle breakdown in response to physical trauma or biochemical disturbance. Necrotic myocytes release myoglobin, a metabolite of which is directly toxic to renal tubules causing ATN. Additionally, ischaemic or necrotic muscle can sequester very large quantities of fluid causing severe dehydration. Significant muscle cell death also releases potassium, phosphate, CK, and urate, which are disproportionately high in rhabdomyolysis. Hyperkalaemia can develop rapidly and is a medical emergency.
Urine is typically ‘Coca-Cola’ coloured due to the presence of myoglobin. Urine dipsticks cannot distinguish this from haemoglobin but the biochemistry lab can.
You should suspect rhabdomyolysis in patients with compartment syndrome or significant limb injuries, anyone who has been on the floor for a long time (frail elderly, alcohol-dependent patients), and following recreational drug use.
CK (often >100,000 U/L), K+, PO43−, urate, urine dip, and urine myoglobin.
Renal failure from rhabdomyolysis can be prevented by early and aggressive fluid regimens driving large-volume diuresis to ‘flush out’ myoglobin and to replace fluid losses in injured muscle. This may require >10 L/day and should only be done in HDU setting. There is limited evidence for urinary alkalinization with sodium bicarbonate to reduce the formation of toxic myoglobin metabolites.
In practice, most patients with rhabdomyolysis have established renal impairment at the time of presentation. In these cases, aggressive fluid resuscitation may still be beneficial but should be done with extreme care due to the risk of fluid overload in the face of falling urine output. Oliguria and hyperkalaemia mandate immediate haemodialysis treatment. Patients usually recover renal function but may remain dialysis dependent for weeks.
Beware that calcium may precipitate with extracellular phosphate causing severe hypocalcaemia. This should be treated only if the patient has symptoms (e.g. tetany or cardiac arrhythmia) due to the risk of further calcium deposition.
Occurs in patients with very cellular/proliferative malignancies such as leukaemias and lymphomas, usually at the initiation of treatment but sometimes spontaneously. Sudden lysis of metabolically active and purine-rich tumour cells massive release of intracellular uric acid (and K+/PO43−/LDH as in rhabdomyolysis) which crystallizes in the renal tubules AKI.
Preventative measures before cancer therapy is started include allopurinol (xanthine oxidase inhibitor) and IV fluids. Rasburicase is a new recombinant urase oxidase which rapidly oxidizes uric acid. This is increasingly used prophylactically.
As in rhabdomyolysis, the combination of falling urine output and hyperkalaemia would prompt emergency haemodialysis. Renal function usually recovers with appropriate management.
Patients with advanced liver disease have a number of problems predisposing them to AKI: ascites and hypoalbuminaemia, spontaneous bacterial peritonitis, shock from oesophageal varices, and drugs such as spironolactone.
A particular condition called hepatorenal syndrome occurs due to renal vasoconstriction in response to a fall in useful circulating volume. It is diagnosed only where no other cause of ATN or kidney disease is identified, and generally confers a poor prognosis.
Optimize fluid balance (CVP monitoring, 20% human albumin solution), treat infections, and stop nephrotoxic drugs. The use of the IV vasopressin analogue terlipressin causes redistribution of circulation via splanchnic vasoconstriction and may reverse renal vasoconstriction. It should not be used in ischaemic heart disease.
If the patient is a candidate for liver transplant then RRT is appropriate. Renal function in hepatorenal syndrome should improve with the restoration of normal liver function but where a patient is established on RRT, combined liver–kidney transplant may be undertaken.
Solutes such as urea and K+ are removed by diffusion across a dialysis membrane, and H2O by osmosis. Ultrafiltration removes additional fluid. Look out for ‘crash landers’ who present at end-stage renal failure without having any pre-dialysis work-up.
• Fast and efficient compared to continuous techniques.
• Does not require active patient involvement.
• Can be done through temporary line.
• In-hospital or satellite units.
• Line infections and other complications of vascular access.
Uses peritoneum as dialysis membrane.
• Gradual/continuous so well tolerated haemodynamically.
• Better fluid and K+ control.
• Home therapy and ‘normal routine’ allows patient empowerment.
• May preserve residual renal function more than haemodialysis.
• Peritoneal dialysis peritonitis.
• Planning/access required with Tenckhoff catheter.
• Encapsulating peritoneal sclerosis.
Kidney transplanted from deceased or living donor usually into iliac fossa.
• Provides more renal function than any form of dialysis.
• Better quality and quantity of life with improved cardiovascular health.
• Relative independence from medical interventions (dialysis, fluid restriction, etc.).
• Complications of immunosuppression (infections, haematological, diabetes, malignancy).
Is appropriate where dialysis is unlikely to improve quality or quantity of life.
• Fewer hospital visits and admissions.
• Ultimately patient will die from renal failure.
• May experience uraemic symptoms and fluid overload.
Ideally this is an elective procedure in a patient with a planned dialysis start, in which case a semi-permanent tunnelled line is inserted. Sometimes, however, a breathless or hyperkalaemic patient requires a temporary vascath for emergency dialysis.
Dual lumen although both are contained within a single tube in the vein and only split after exiting the skin. Both sit in a central vein but one lumen is called ‘arterial’ as it removes blood from the body. Usually about 24 cm long and 12 French gauge.
• Right internal jugular vein (RIJV): follows a shorter straight line to the junction between SVC and right atrium. Cleaner than femoral.
• Left internal jugular vein (LIJV): longer more tortuous course hence higher resistance to flow (Poiseuille’s law) and more opportunity for wire to take a wrong turn.
• Femoral: often easiest in an emergency and compressible if patient is anticoagulated/coagulopathic. Less clean and may restrict mobility and predispose to DVT.
• Subclavian: avoided by nephrologists where possible due to risk of causing central venous stenosis.
• Consent patient for risk of bleeding/infection/pneumothorax (if jugular or subclavian) and misplaced line.
• Strict adherence to aseptic technique is critical for central venous lines especially semi-permanent tunnelled lines. Vancomycin frequently given post procedure.
• US guidance is recommended by NICE for central venous cannulation. It is particularly valuable in chronic renal patients with previous lines/thrombosed veins.
• Local anaesthetic to skin. Aspirate before injection to avoid bolus of IV lignocaine.
• Prepare the line by flushing lumens with normal saline to avoid air embolism.
• Seldinger technique: the vein is cannulated under US guidance with a wide-bore needle until venous blood is aspirated. A guide wire is inserted through the introducer needle which is then removed. Skin and soft tissue are then dilated using sheaths inserted over the guide wire. Dilators are removed and the vascath inserted over the guide wire, which must then itself be withdrawn. Venous blood should be aspirated freely through both lumens which are then flushed with saline and locked with heparin to reduce clot formation. Non-absorbable sutures are used to anchor the line to skin.
• CXR to confirm position at SVC/right atrial junction and exclude pneumothorax before using the line. Femoral line does not require imaging and can be used immediately.
• Carotid/femoral arterial cannulation: withdraw immediately and compress for several minutes to avoid haematoma and to achieve haemostasis.
• Pneumothorax: seek expert help.
Usually an elective procedure in patients with nephrotic syndrome or AKI/CKD, of unknown cause. Patient should be sufficiently mobile/fit to lie on their front for up to 30 min and be able to cooperate with instructions such as breath holding.
• Control BP to reduce bleeding risk (usually <160/100 mmHg).
• US to exclude obstruction/tumour or single kidney.
• Normal platelets and clotting. Ask about warfarin/antiplatelet drugs.
• Consent patient for risk of visible haematuria (<5%; see Fig. 21.2), urinary clot retention (<2%), bleeding requiring blood transfusion (<1%), further intervention (e.g. embolization/nephrectomy (<0.5%)).
• Patient lies in supine position often with pillow beneath abdomen to encourage kyphosis.
• Skin cleaned and local anaesthetic infiltrated to level of kidney under US guidance.
• Biopsy needle advanced to kidney (with US). Ask patient to hold breath to reduce movement of kidney. Biopsy gun will retrieve sliver of renal tissue ~1 × 10 mm. Usually two cores taken.
• Bed rest for 4–6 hours after with frequent BP/HR monitoring and visual inspection of urine.
• Bleeding: interventions as listed previously.
• Upper or lower tract obstruction due to clot and need for nephrostomy/stent or bladder irrigation/catheter respectively.
• Arteriovenous fistula formation at biopsy site; usually only a problem in transplanted (i.e. single) kidney where significant shunt may require embolization.
Fig. 21.2 Causes of frank haematuria. AVM, arteriovenous malformation. Reproduced with permission from Piers Page and Greg Skinner, Emergencies in Clinical Medicine, 2008, Oxford University Press.
Renal patients are frequently asked to help with clinical exams; they have chronic conditions, stable clinical signs, and regular hospital visits. The examination routines are covered elsewhere, but here are a few things to look out for:
• ADPKD: large, bilateral, ballotable masses in the flanks. Often associated with polycystic liver too.
• DM: finger pricks from BM testing, insulin injection marks on abdomen, visual impairment/guide dog, sugar-free drink on table, Medic Alert bracelet.
• Alport’s syndrome: hearing aid.
• Nephrectomy scars: flanks, often well healed and concealed by skin folds.
• Haemodialysis: arteriovenous fistula especially at wrist or elbow. Is there a thrill? Has it been needled recently (plaster/scab)? Defunct fistula elsewhere? Haemodialysis catheters, usually tunnelled over chest wall inserted into jugular vein. Look for scars near clavicle. Some haemodialysis patients have central vein obstruction causing signs of SVC obstruction or dilated collateral veins over chest wall.
• Peritoneal dialysis: Tenckhoff catheter exiting few cm lateral to umbilicus, tunnelled to midline, and small midline scar. Offer to check exit site but do not remove dressing without instruction due to infection risk. Catheters are removed at transplant, so look for scars.
• Renal transplant: smooth palpable mass beneath ‘hockey stick’ scar in iliac fossa. There may be a failed graft on other side. Listen for bruit.
• Fluid overload: look for peripheral oedema (including ankles and sacrum), and raised JVP.
• Hyperparathyroidism: parathyroidectomy scar (identical to thyroidectomy).
• Pruritus: look for linear scratch marks (excoriations) especially limbs/torso.
• Steroids: bruising/moon face/buffalo hump/diabetes mellitus/acne.
• Tacrolimus: fine, resting tremor.
• Ciclosporin: hirsutism, gum hypertrophy.
As many as one in five patients on IV fluids and electrolytes suffer complications or morbidity due to their inappropriate administration.
However, here are some general tips from the NICE IV fluid therapy guidelines:
• If the gut works—use it! Consider using oral or nasogastric rehydration before IV. Stop IV fluids as soon as they are no longer needed.
• Prescriptions should include the type, rate, and volume of the fluid to be given (e.g. ‘500 mL 0.9% sodium chloride IV over an hour’).
1. Resuscitation (500 mL boluses of crystalloid).
4. Redistribution (is fluid leaking into their gut/interstitium?).
5. Reassessment (pulse, BP, mucous membranes, skin turgor, capillary refill time, mental status. Keep urine output >0.5 mL/kg/hour (only if renal failure not present)).
• Do not forget to consider all other sources of fluid and electrolyte intake (IV or enteral), including drugs, IV nutrition, blood, and blood products.
• All patients on IV fluids must have a fluid balance chart and daily review including body weight and U&E.
When on the wards, take time to look at the bags of fluid and what they contain. Fluids are treated as a prescribed drug so it is important you know what is in them (see comparison table of different IV fluids at 
www.frca.co.uk/article.aspx?articleid=295).
• HR increases will be masked in the elderly and by beta blockers.
• Interpret BP in the light of any history of hypertension.
• Oliguria may be masked by diuretics.
• Capillary refill time is also by a cold environment, hypothermia, pain, and anxiety.
• Never infuse fluids containing >5 mmol/L potassium rapidly (can cause arrhythmias).