Acute kidney injury is a core exam topic because it tests a clear definition, a logical causal framework, and a management approach that hinges on finding and treating the cause. This guide covers AKI as examiners frame them, to the current NICE standard (NG148) and the KDIGO staging system. Follow current guidance and local protocols in practice; this reflects guidance as of mid-2026.
What AKI is
Acute kidney injury is an abrupt decline in kidney function over hours to days, reflected in a rising creatinine, a falling urine output, or both. It is common in hospital, frequently avoidable, and associated with longer admissions, chronic kidney disease and increased mortality — which is why early recognition and prevention are emphasised. AKI is often clinically silent and detected on blood tests, but it can present with reduced or absent urine output, fluid overload and breathlessness, confusion, or the symptoms of the underlying cause. Many cases arise in patients already in hospital for another illness, particularly with sepsis, hypovolaemia or nephrotoxic drugs — which is why monitoring of at-risk patients is central to prevention.
Definition and staging
NICE detects AKI using any one of three criteria: a rise in serum creatinine of 26 micromol/L or more within 48 hours; a 50% or greater rise in creatinine known or presumed to have occurred within the past 7 days; or a fall in urine output to less than 0.5 mL/kg/hour for more than 6 hours. The KDIGO system then stages severity: stage 1 is a 1.5 to 1.9-fold rise in creatinine; stage 2 is a 2 to 2.9-fold rise; and stage 3 is a threefold rise, a creatinine of 354 micromol/L or above, or the need for renal replacement therapy. Staging matters because higher stages carry worse outcomes, and any rise should prompt a search for the cause.
The causal framework
Examiners expect you to classify the cause into three groups, because this drives the work-up:
- Pre-renal: reduced kidney perfusion — hypovolaemia (haemorrhage, dehydration, diarrhoea and vomiting), sepsis, heart failure, and drugs that reduce perfusion such as NSAIDs and ACE inhibitors or ARBs. This is the commonest category, and reversible if perfusion is restored before damage sets in.
- Intrinsic (renal): damage to the kidney itself — acute tubular necrosis (the commonest intrinsic cause, from prolonged ischaemia or nephrotoxins), glomerulonephritis, acute interstitial nephritis (often drug-induced), and vascular causes.
- Post-renal: obstruction to urine flow — stones, an enlarged prostate, pelvic tumours, or a blocked catheter. This matters because it is often quickly reversible by relieving the obstruction.
Investigations
Alongside serial U&Es, the key tests are a urine dipstick (blood and protein point towards an intrinsic glomerular cause) and a renal ultrasound to look for obstruction, arranged urgently if obstruction is suspected. Review the fluid balance and observations, screen for sepsis, and send further tests for intrinsic causes (such as an autoimmune screen) where the picture suggests it. Always check the potassium and an ECG, because hyperkalaemia is the dangerous early complication. A careful drug history and an assessment of volume status — pulse, blood pressure, jugular venous pressure, skin turgor and fluid charts — often point to the cause before any test returns.
Management
There is no specific drug that reverses AKI; management is supportive and directed at the cause:
- Treat the cause: restore circulating volume in pre-renal AKI, treat sepsis, and relieve obstruction in post-renal AKI.
- Optimise fluids and perfusion: careful fluid resuscitation in the hypovolaemic patient, with equal care not to overload the patient who is anuric or fluid-overloaded.
- Stop the nephrotoxins: hold NSAIDs, ACE inhibitors and ARBs, aminoglycosides and other nephrotoxic drugs, and review doses of renally-cleared drugs. This is often summarised in "sick day" guidance.
- Monitor and treat complications: hyperkalaemia, fluid overload, metabolic acidosis and uraemia.
Most AKI, especially pre-renal, recovers if the cause is corrected promptly; the role of the generalist is timely recognition, fluid and drug review, and escalation rather than waiting.
When dialysis is needed
Urgent renal replacement therapy is indicated for complications refractory to medical treatment, remembered by the mnemonic AEIOU: severe Acidosis, refractory Electrolyte disturbance (especially hyperkalaemia), Intoxication with certain poisons, fluid Overload causing pulmonary oedema, and Uraemic complications such as pericarditis or encephalopathy.
High-yield exam points and traps
- Know the definition precisely: a creatinine rise of 26 micromol/L in 48 hours, a 50% rise in 7 days, or urine output below 0.5 mL/kg/hour for over 6 hours.
- Pre-renal is the commonest category, and acute tubular necrosis the commonest intrinsic cause.
- Always exclude obstruction with a renal ultrasound and a bladder assessment — it is the most readily reversible cause.
- Hyperkalaemia is the dangerous early complication: check the potassium and an ECG.
- Stop nephrotoxic drugs — NSAIDs, ACE inhibitors and ARBs are the usual culprits.
- The indications for dialysis (AEIOU) are about complications refractory to treatment, not the creatinine number alone.
- Catheterise and image early if obstruction is plausible — a blocked catheter or urinary retention is an easily missed, easily fixed cause.
A few common questions
How is AKI defined? By any one of: a creatinine rise of 26 micromol/L or more in 48 hours, a 50% or greater rise within 7 days, or urine output below 0.5 mL/kg/hour for more than 6 hours.
What are the causes of AKI? Pre-renal (reduced perfusion, the commonest), intrinsic (kidney damage, often acute tubular necrosis), and post-renal (obstruction).
What investigations are essential? Serial U&Es, a urine dipstick, a renal ultrasound to exclude obstruction, and a potassium with an ECG; further tests for intrinsic causes as indicated.
When is dialysis needed in AKI? For complications refractory to medical treatment — severe acidosis, refractory hyperkalaemia, certain intoxications, fluid overload, or uraemic complications (the AEIOU mnemonic).
Which drugs should be stopped in AKI? Nephrotoxic and perfusion-reducing drugs — NSAIDs, ACE inhibitors and ARBs, aminoglycosides — and renally-cleared drugs reviewed for dose.
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