Abrupt decline in kidney function defined by creatinine rise or oliguria. Frequently iatrogenic; preventable in many cases.
⚠ Red flags
- K⁺ >6.5 — cardiac arrhythmia risk
- pH <7.1 — severe acidosis
- Pulmonary oedema unresponsive to diuretics
- Doubling of creatinine in <24h
- Anuria
Diagnostic criteria
Clinical
- Reduced urine output (<0.5 mL/kg/h ≥6h)
- New oedema, fluid overload, or uraemic features (encephalopathy, pericarditis)
Investigations
- Creatinine ≥26.5 µmol/L rise within 48h, OR
- Creatinine ≥1.5× baseline within 7 days
- Urine output <0.5 mL/kg/h for ≥6h
Scoring tools
- KDIGO AKI staging (1–3)
- RIFLE / AKIN criteria (legacy)
Investigations
Essential
- Creatinine trend, eGFR, U&E (especially K⁺)
- Urinalysis: protein, blood, casts
- FBC, CRP, coagulation
- ABG / VBG (acidosis)
- Renal USS within 24h to exclude obstruction
Optional
- Urine sodium / FENa / FEUrea (pre-renal vs intrinsic)
- Autoimmune screen (ANA, ANCA, anti-GBM, complement) if intrinsic
- Myoglobin / CK if rhabdomyolysis
- Renal biopsy if intrinsic AKI of unclear cause
Management
Acute
- Treat underlying cause: rehydrate (pre-renal), relieve obstruction (post-renal), specific therapy (intrinsic)
- Stop nephrotoxins: NSAIDs, ACEi/ARB, aminoglycosides, contrast
- Hyperkalaemia: calcium gluconate 10 mL 10% IV; insulin-dextrose; salbutamol nebs; consider RRT
- Acidosis: bicarbonate if pH <7.1 and adequate ventilation
- RRT indications: refractory hyperkalaemia/acidosis, fluid overload, uraemic complications (AEIOU)
Long-term
- Reassess renal function at 90 days post-AKI for CKD
- Medication reconciliation — restart ACEi/ARB cautiously once stable
Non-pharmacological
- Strict fluid balance with daily weights
- Renal-friendly diet (potassium, phosphate, salt restriction)
- Avoid hospital-acquired AKI: medication review, contrast stewardship
Pharmacological
| Drug | Dose | Notes |
|---|---|---|
| Calcium gluconate 10% | 10 mL IV over 10 min | Cardiac stabilisation in hyperkalaemia ECG changes. |
| Insulin + dextrose | 10 units actrapid + 50 mL 50% dextrose IV | Drives K⁺ intracellularly; recheck glucose at 1h. |
| Salbutamol | 10–20 mg nebulised | Adjunct K⁺ shift therapy. |
| Sodium bicarbonate | 1.26% IV per pH/lactate | Severe acidosis pH <7.1. |
| Furosemide | 40–80 mg IV | Only if clear fluid overload — does not improve AKI per se. |
Monitoring
- Hourly urine output and fluid balance
- U&E and venous gas every 4–6h while unstable
- Daily weight
- ECG monitoring if K⁺ >6 or symptomatic
Referral criteria
- Stage 3 AKI
- Pulmonary oedema unresponsive to diuretics
- Refractory hyperkalaemia or acidosis
- Suspected intrinsic AKI of unclear cause
Complications
- Hyperkalaemia and arrhythmia
- Pulmonary oedema
- Uraemic encephalopathy / pericarditis
- Progression to CKD
- Increased long-term cardiovascular mortality
Special populations
- Pregnancy
- Pre-eclampsia, HELLP, AFLP, septic abortion as obstetric causes. Engage obstetrics + nephrology jointly.
- Renal impairment
- Pre-existing CKD increases AKI risk; baseline creatinine essential for staging.
- Hepatic impairment
- Hepatorenal syndrome — terlipressin + albumin; transplant assessment.
- Elderly
- Often multifactorial (sepsis + drugs + dehydration). Frailty assessment guides RRT decisions.
- Paediatric
- Use paediatric KDIGO / pRIFLE; weight-based fluid management; involve paediatric nephrology.