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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- AKI definition (KDIGO): rise in creatinine ≥26.5 μmol/L in 48 h, OR ≥1.5× baseline in 7 days, OR urine output <0.5 mL/kg/h for >6 h
- Pre-renal (~60%): hypovolaemia, sepsis, heart failure, drugs (ACEi, NSAIDs, diuretics). Intrinsic (~35%): ATN, glomerulonephritis, interstitial nephritis. Post-renal (~5%): obstruction (stones, BPH, tumour)
- First step: assess fluid status and perform renal USS (exclude obstruction)
- Stop nephrotoxic drugs (ACEi/ARB, NSAIDs, metformin, gentamicin)
- Indications for urgent dialysis: refractory hyperkalaemia, severe acidosis, pulmonary oedema, uraemic encephalopathy/pericarditis, toxin removal
Overview
Acute kidney injury is a rapid deterioration in renal function resulting in accumulation of waste products and disordered fluid/electrolyte homeostasis. It is classified by the KDIGO staging system into 3 stages of increasing severity. The aetiology is categorised as pre-renal (reduced renal perfusion), intrinsic renal (parenchymal damage), or post-renal (urinary tract obstruction). Pre-renal AKI is the commonest cause and is usually reversible with prompt fluid resuscitation. AKI is common in hospitalised patients (affecting ~15% of admissions) and is associated with significant morbidity and mortality.
Epidemiology
AKI affects approximately 13–18% of hospital admissions. Mortality in severe AKI requiring renal replacement therapy is ~50%. Risk factors include age >65, CKD, diabetes, heart failure, liver disease, sepsis, nephrotoxic drugs, hypovolaemia, urological obstruction, and recent surgery (especially cardiac). Hospital-acquired AKI carries worse prognosis than community-acquired. Recovery depends on cause — pre-renal AKI typically recovers fully; intrinsic renal damage may lead to CKD.
Clinical Features
Symptoms
Reduced urine output (oliguria <400 mL/day or anuria)
Nausea, vomiting, anorexia
Confusion, drowsiness (uraemic encephalopathy)
May be asymptomatic — detected on routine bloods
Symptoms of underlying cause: sepsis, dehydration, urinary retention
Signs
Dehydration: dry mucous membranes, reduced skin turgor, tachycardia, postural hypotension
Fluid overload: peripheral oedema, raised JVP, pulmonary crackles
Palpable bladder (post-renal obstruction)
Uraemic frost (severe — extremely rare)
Asterixis (uraemic flap)
Investigations
First-line
U&Es (creatinine, urea, potassium)Rising creatinine defines AKI. Hyperkalaemia is the most immediately dangerous electrolyte abnormality
Urinalysis (dipstick)Blood + protein suggests intrinsic renal disease (glomerulonephritis). Leucocytes/nitrites suggest UTI
Renal USSExclude obstruction (hydronephrosis) — all AKI patients should have USS within 24 h. Small kidneys suggest pre-existing CKD
Fluid balance assessmentClinical assessment + fluid chart. Catheterise to accurately monitor urine output
Second-line
VBG/ABGMetabolic acidosis (low bicarbonate) — severity guides management and dialysis decision
FBC, CRP, blood culturesSepsis screen — infection is a common precipitant
CKIf rhabdomyolysis suspected (crush injury, prolonged immobility, statins)
Urine protein:creatinine ratio (PCR)Quantify proteinuria if dipstick positive for protein
Specialist
Immunology screenANA, ANCA, anti-GBM, complement — if vasculitis or glomerulonephritis suspected
Renal biopsyIf intrinsic renal disease suspected and cause unclear — guides immunosuppressive treatment
Myeloma screenSerum protein electrophoresis, Bence Jones protein — in older patients with AKI and bone pain/anaemia/hypercalcaemia
Management
NICE NG148 (Acute kidney injury), 20191
Immediate management
- Stop nephrotoxic drugs: ACEi/ARB, NSAIDs, aminoglycosides, metformin
- Assess fluid status: if hypovolaemic → IV fluid challenge (250–500 mL crystalloid over 15–30 min, reassess)
- If fluid overloaded → restrict fluids, consider furosemide
- Treat hyperkalaemia urgently if K⁺ >6.5 or ECG changes: calcium gluconate (cardioprotection) → insulin + dextrose → salbutamol nebuliser
- Catheterise to monitor urine output accurately
2
Treat the underlying cause
- Pre-renal: fluid resuscitation, treat sepsis, optimise cardiac output
- Post-renal: urinary catheter (bladder outflow obstruction), nephrostomy (ureteric obstruction)
- Intrinsic: depends on cause — antibiotics for pyelonephritis, immunosuppression for vasculitis/GN, IV fluids for rhabdomyolysis (target UO >200 mL/h)
3
Indications for renal replacement therapy (dialysis)
- Refractory hyperkalaemia (not responding to medical management)
- Severe metabolic acidosis (pH <7.1)
- Pulmonary oedema refractory to diuretics
- Uraemic complications: encephalopathy, pericarditis, bleeding
- Drug/toxin removal (lithium, ethylene glycol, methanol)
- Mnemonic: AEIOU — Acidosis, Electrolytes (K⁺), Intoxication, Overload (fluid), Uraemia
4
Recovery and follow-up
- Monitor U&Es daily during acute phase
- Gradual recovery expected for pre-renal AKI
- Follow up at 3 months with U&Es — some patients develop CKD
- Educate about sick day rules: stop ACEi/ARB, metformin, NSAIDs during acute illness with dehydration
Complications
- Hyperkalaemia: Most immediately life-threatening — causes cardiac arrhythmias and arrest
- Metabolic acidosis: Impaired acid excretion — may require bicarbonate or RRT
- Fluid overload and pulmonary oedema: If aggressive fluid resuscitation without monitoring output
- Uraemia: Encephalopathy, pericarditis, platelet dysfunction (bleeding)
- Progression to CKD: AKI is an independent risk factor for developing CKD
UKMLA Exam Tips
- 1First step in AKI: STOP nephrotoxics (ACEi, NSAIDs, metformin) and assess volume status
- 2Renal USS within 24 h for ALL AKI — exclude obstruction (the readily reversible cause)
- 3Hyperkalaemia >6.5 or ECG changes: calcium gluconate FIRST (cardioprotection), then insulin+dextrose to shift K⁺
- 4Dialysis indications (AEIOU): Acidosis, Electrolytes, Intoxication, Overload, Uraemia
- 5Pre-renal AKI: urea rises disproportionately to creatinine (urea:creatinine ratio >100:1)
- 6Sick day rules: patients on ACEi/ARB/metformin should stop these during acute dehydrating illness
practicetest your knowledge on akiApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — renal and beyond.
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