Key Facts

AKI is extremely common and carries significant mortality. It is often preventable and early recognition with appropriate management can reverse most cases. The key is to identify the cause (pre-renal, intrinsic, or post-renal), stop nephrotoxins, and treat urgently.

Epidemiology

AKI affects 13-18% of hospitalised patients and is increasing in incidence. Community-acquired AKI accounts for ~50% of cases. In-hospital mortality: Stage 1 ~10%; Stage 2 ~20%; Stage 3 ~25-30%. AKI is associated with increased length of stay, ICU admission, and progression to CKD.

Aetiology

Pre-renal (55%):

• Hypovolaemia: Dehydration, haemorrhage, burns
• Hypotension: Sepsis, cardiogenic shock
• Drugs: ACEi/ARB, NSAIDs (reduce GFR)

Intrinsic renal (35%):

• Acute tubular necrosis (ATN): Ischaemic (prolonged pre-renal) or nephrotoxic (aminoglycosides, contrast, myoglobin)
• Glomerulonephritis: ANCA vasculitis, anti-GBM, lupus nephritis
• Acute interstitial nephritis: Drug-induced (penicillins, NSAIDs, PPIs)
• Rhabdomyolysis: Crush injury, statins, seizures, heat stroke

Post-renal (10%):

• Ureteric obstruction: Stones, tumour, retroperitoneal fibrosis
• Bladder outflow obstruction: BPH, prostate cancer, urethral stricture

Pathophysiology

Pre-renal AKI results from reduced renal perfusion. If sustained, it progresses to ATN (intrinsic). ATN involves necrosis of tubular epithelial cells from ischaemia or direct toxicity, leading to loss of concentration ability, impaired sodium reabsorption, and cast formation. Post-renal AKI results from increased hydrostatic pressure proximal to obstruction, impairing glomerular filtration.

Clinical Features

• Often asymptomatic — detected on blood tests (AKI e-alert)
• Reduced urine output (<0.5mL/kg/hr for >6h)
• Fluid overload: Peripheral oedema, pulmonary oedema, raised JVP
• Uraemia: Nausea, vomiting, confusion, pruritus, pericarditis
• Features of underlying cause: Fever (infection), rash (vasculitis), loin pain (obstruction)

Red Flags

• Anuria — complete obstruction or severe intrinsic disease
• Hyperkalaemia >6.0 mmol/L — life-threatening arrhythmia risk
• Pulmonary oedema — urgent diuresis or dialysis
• Uraemic encephalopathy/pericarditis — emergency dialysis indication
• Active urinary sediment (red cell casts, protein) — suggests glomerulonephritis; urgent nephrology input

Bedside

• Urine output: Catheterise — measure hourly; <0.5mL/kg/hr is significant
• Fluid status: JVP, peripheral oedema, lung crackles, blood pressure
• Bladder scan: Post-void residual — exclude urinary retention
• Urine dipstick: Blood + protein = glomerular disease; leucocytes/nitrites = infection
• ECG: Hyperkalaemia changes (peaked T waves, wide QRS, sine wave)

Bloods

• U&Es: Creatinine (serial), potassium, sodium, urea
• FBC: Anaemia (CKD, HUS), eosinophilia (interstitial nephritis)
• CRP: Infection/inflammation
• CK: Rhabdomyolysis (>5× ULN)
• LDH, reticulocytes, haptoglobin, blood film: If haemolytic uraemic syndrome (HUS/TTP) suspected
• Immunology: ANCA, anti-GBM, ANA, complement (C3/C4) — if glomerulonephritis suspected

Imaging

• Renal USS: Within 6 hours if obstruction suspected (hydronephrosis), within 24h for all AKI

Special Tests

• Urine sodium and osmolality: Pre-renal (Na⁺ <20, osmolality >500) vs ATN (Na⁺ >40, osmolality <350)
• Urine protein:creatinine ratio (uPCR): Quantify proteinuria
• Renal biopsy: If intrinsic cause unclear and diagnosis would change management

Non-pharmacological

• Fluid assessment: Hypovolaemic → IV crystalloid bolus; euvolaemic → maintenance; fluid overloaded → restrict and consider diuretics
• Stop nephrotoxins: 'Hold the DAMN drugs' — Diuretics (if hypovolaemic), ACEi/ARB, Metformin, NSAIDs; also aminoglycosides, contrast
• Catheterise: Monitor urine output; relieve retention if post-renal
• Daily U&Es: Track trajectory

Pharmacological

• IV fluid resuscitation: 250-500mL 0.9% NaCl bolus if hypovolaemic; reassess response
• Hyperkalaemia management (if K⁺ >6.0):
  • Calcium gluconate 10% 30mL IV (cardiac membrane stabilisation)
  • Insulin 10 units + 25g glucose IV (shift K⁺ intracellularly)
  • Salbutamol 10-20mg nebulised
  • Calcium resonium 15g PO/PR (slow K⁺ removal)
  • Sodium bicarbonate 8.4% 50mL if acidotic
• IV furosemide: 40-250mg for fluid overload (only if not hypovolaemic)
• Treat underlying cause: Antibiotics for sepsis, hydration for rhabdomyolysis (target UO >200mL/hr)

Surgical/Interventional

• Nephrostomy or ureteric stent: For obstructive uropathy
• Catheter insertion: For bladder outflow obstruction
• Renal replacement therapy (dialysis): For refractory hyperkalaemia, acidosis, fluid overload, uraemic complications, certain toxins (AEIOU)

Referral Criteria

• AKI stage 3 — nephrology referral
• Suspected glomerulonephritis/vasculitis — urgent nephrology
• Obstruction requiring intervention — urology
• Indications for dialysis — renal/ICU team
• AKI with unknown cause — nephrology input within 24h

• Pre-renal AKI: Usually reversible within 24-48h with appropriate fluid management
• ATN: Recovery typically over 1-3 weeks; some progress to CKD
• Post-renal: Excellent recovery if obstruction relieved promptly (within 48h)
• Hospital mortality: Stage 1 ~10%, Stage 2 ~20%, Stage 3 ~25-30%
• CKD progression: ~20% of AKI survivors develop CKD within 5 years; ~5% require long-term dialysis
• Post-obstructive diuresis: Can cause severe polyuria — monitor and replace fluids

KDIGO AKI Staging

Indications for Emergency Dialysis (AEIOU)