Acute kidney injury
Exam Tips
- Use KDIGO-style criteria accurately in OSCE/viva: creatinine rise >=26 micromol/L in 48 hours, or >=1.5x baseline in 7 days, or oliguria <0.5 mL/kg/hour for >6 hours.
- Always structure causes as pre-renal, intrinsic, post-renal and state that mixed aetiology is common in real patients.
- In emergency stations, treat hyperkalaemia first (ECG + IV calcium, insulin/glucose, salbutamol) while addressing AKI cause.
- A catheterised urine output chart is both diagnostic and therapeutic in suspected obstructive AKI.
- Mention nephrotoxin review explicitly (NSAIDs, ACEi/ARB, diuretics, aminoglycosides, contrast) to gain management marks.
- Image reference: see a standard 'Pre-renal vs intrinsic vs post-renal AKI pathway' diagram and a nephron injury schematic for ATN/AIN pattern recognition.
Definition
Acute kidney injury (AKI) is a clinical syndrome of rapid decline in kidney function, developing over hours to days, that leads to impaired excretion of waste and loss of fluid, electrolyte, and acid-base homeostasis. It is diagnosed by dynamic changes in serum creatinine and/or urine output rather than a single static blood result, and includes a spectrum from mild injury to severe kidney failure.
Pathophysiology
AKI usually reflects one or more overlapping mechanisms: pre-renal hypoperfusion, intrinsic renal parenchymal injury, and post-renal urinary obstruction. In pre-renal states (for example hypovolaemia, sepsis, heart failure), reduced renal blood flow lowers glomerular filtration pressure; if prolonged, ischaemia causes tubular cell injury and acute tubular necrosis (ATN). Intrinsic AKI includes ATN, acute interstitial nephritis (often drug-related), glomerular inflammation, and vascular injury, all of which reduce filtration and impair tubular transport. Post-renal obstruction increases intratubular pressure, reducing net filtration gradient; bilateral obstruction or obstruction in a solitary functioning kidney can cause abrupt severe AKI. Neurohormonal activation (RAAS, sympathetic tone), endothelial dysfunction, and inflammation amplify injury and can lead to multi-organ effects.
Risk Factors
- Age 65 years or older
- Pre-existing chronic kidney disease (especially eGFR <60 mL/min/1.73 m2)
- Previous episode of AKI
- Sepsis or severe acute illness
- Hypovolaemia, dehydration, hypotension, or poor oral intake
- Heart failure, liver disease, diabetes mellitus (particularly with proteinuria)
- Urological obstruction risk (for example prostate enlargement, stones, pelvic malignancy)
- Recent nephrotoxin exposure: NSAIDs, ACE inhibitors, ARBs, diuretics, aminoglycosides, iodinated contrast
- Cancer and anticancer therapy
- Immunocompromised state or major comorbidity burden
Clinical Features
Symptoms
- Often asymptomatic early on
- Reduced urine output (oliguria) or dark/concentrated urine
- Nausea, vomiting, anorexia, diarrhoea
- Thirst, dizziness, reduced intake (dehydration features)
- Fatigue, lethargy, confusion, drowsiness
- Breathlessness if fluid overload develops
Signs
- Oliguria (<0.5 mL/kg/hour) or anuria
- Clinical dehydration: dry mucosae, poor skin turgor, postural hypotension, tachycardia
- Hypotension or septic physiology
- Peripheral oedema, raised JVP, basal crackles/pulmonary oedema
- Uraemic features in severe disease (encephalopathy, pericardial rub)
- Features suggesting obstruction: palpable bladder, loin pain, enlarged prostate
Investigations
Management
Lifestyle Modifications
- Immediate safety-net hydration plan and monitored fluid intake/output (daily weights, fluid balance chart)
- Sick-day advice in high-risk patients: temporarily stop ACE inhibitor/ARB/NSAID/diuretics during vomiting, diarrhoea, fever, or poor intake until reviewed
- Early escalation for reduced urine output, breathlessness, or confusion; avoid over-the-counter NSAIDs
Pharmacological Treatment
Fluid resuscitation and haemodynamic optimisation
- Sodium chloride 0.9% IV bolus 250-500 mL over 15-30 minutes, reassess and repeat as needed
- Balanced crystalloid (for example Hartmann's solution) can be used depending on biochemical profile
Use careful reassessment (pulse, BP, JVP, lung exam, urine output, lactate). Avoid fluid overload in heart failure/advanced CKD; give smaller aliquots in frail or fluid-sensitive patients.
Hyperkalaemia emergency treatment
- Calcium gluconate 10% 10 mL IV over 2-5 minutes (cardiac membrane stabilisation)
- Insulin (soluble insulin, e. g. Actrapid) 10 units IV with glucose 25 g IV (e. g. 50 mL of 50% glucose or 125 mL of 20% glucose) over 15-30 minutes
- Salbutamol nebulised 10-20 mg as adjunct potassium-shifting therapy
Calcium does not lower potassium; it buys time. Recheck potassium and ECG promptly; monitor capillary glucose for at least 6 hours after insulin/glucose to detect hypoglycaemia. Urgent renal input if refractory, severe, or recurrent hyperkalaemia.
Diuretics for fluid overload (not for kidney recovery)
- Furosemide 40-80 mg IV (or oral if appropriate), titrate to response
Use only if volume overloaded and not hypovolaemic. Loop diuretics do not treat the underlying AKI and can worsen pre-renal AKI if used in dehydration.
Medication optimisation and nephrotoxin avoidance
- Stop NSAIDs (e. g. ibuprofen, naproxen)
- Temporarily withhold ACE inhibitors (e. g. ramipril) and ARBs (e. g. losartan) during active AKI
- Avoid/limit aminoglycosides (e. g. gentamicin) where alternatives exist; if unavoidable, use levels-guided dosing
- Dose-adjust renally cleared medicines (for example low molecular weight heparin, opioids, many antibiotics)
Safety warnings: review metformin (risk of lactic acidosis in severe AKI), potassium-sparing diuretics (hyperkalaemia risk), and contrast exposure. In septic shock, do not delay life-saving antibiotics while adjusting dose.
Renal replacement support in severe AKI context
- Anticoagulation during haemodialysis/haemofiltration as per renal unit protocol (e. g. unfractionated heparin or citrate-based circuit anticoagulation)
Indications include refractory hyperkalaemia, severe acidosis, fluid overload causing pulmonary oedema, uraemic complications, or toxin removal needs. Initiate with nephrology/critical care.
Surgical / Interventional
- Urgent bladder catheterisation for suspected lower urinary tract obstruction
- Upper tract decompression with ureteric stent or percutaneous nephrostomy for obstructive uropathy
- Renal biopsy in selected intrinsic AKI when diagnosis is uncertain and will alter management
Complications
- Hyperkalaemia causing life-threatening arrhythmias or cardiac arrest
- Metabolic acidosis with haemodynamic instability
- Fluid overload leading to pulmonary oedema and heart failure exacerbation
- Uraemia (encephalopathy, pericarditis, neuropathy)
- Electrolyte disturbances: hyperphosphataemia, hypocalcaemia, dysnatraemia
- Progression to chronic kidney disease, end-stage kidney disease, and recurrent AKI
- Higher long-term cardiovascular risk (heart failure, myocardial infarction, stroke)
Prognosis
Prognosis is strongly stage- and context-dependent: mild AKI can recover fully, but mortality rises with increasing AKI severity and with hospital-acquired disease. UK data show AKI is common in emergency admissions and associated with substantial short-term mortality; many survivors have incomplete renal recovery at 90 days and increased risk of chronic kidney disease, cardiovascular events, and future AKI episodes. Presence of baseline CKD, older age, and recurrent or prolonged AKI worsens long-term outcomes.
Sources & References
🏥BMJ Best Practice(2)
✅NICE Guidelines(1)
- Acute kidney injury[overview]
📖Textbook References(20)
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 211)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 262)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 396)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 401)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 829, 830)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 374)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 391)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 391)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1346)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 735)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1368)[context]
- Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 439)[context]
- Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 427, 428)[context]
- Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 427)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 874)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 866)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 858)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 96)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 308)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 153)[context]