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ukmla 2026

Acute Kidney Injury

Rapid decline in renal function over hours to days, defined by rising creatinine and/or falling urine output — classified as pre-renal, intrinsic, or post-renal

Review date
reviewed 2026-04-05
Reading time
7 min read
Author
Dr Kola Tytler MBBS CertHE MBA MSt MRCGP
Renal & Urologycommonacute
On this page
Condition details
Renal & Urology
common
7 min read
reviewed 2026-04-05
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About This Page

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.

Key points

  • 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), 2019
1
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

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regional clinical guidance

Acute Kidney Injury: guidance by region

Recommendations, thresholds and pathways can differ. Open the page written for the jurisdiction you need.

United StatesAcute kidney injury recognition and initial managementRenal · reviewed 2026-08-20CanadaAcute kidney injury (AKI): evidence and source overviewRenal · reviewed 2026-08-20AustraliaAcute kidney injury (AKI)Renal · reviewed 2026-08-20

Verified Sources & References

NICE NG148 — Acute kidney injury
UK Renal Association AKI Guidelines
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