Definition and stages (KDIGO)
AKI is any of:
- A rise in creatinine of 26.5 µmol/L or more within 48 hours
- A rise to 1.5 times baseline or more within 7 days
- Urine output below 0.5 mL/kg/h for 6 hours
| Stage | Creatinine | Urine output |
|---|---|---|
| 1 | 1.5–1.9 × baseline, or rise of 26.5 µmol/L or more | Below 0.5 mL/kg/h for 6–12 hours |
| 2 | 2.0–2.9 × baseline | Below 0.5 mL/kg/h for 12 hours or more |
| 3 | 3 × baseline or more, creatinine 354 µmol/L or more, or dialysis started | Below 0.3 mL/kg/h for 24 hours, or no urine for 12 hours |
Causes
| Type | Causes |
|---|---|
| Prerenal | Diarrhoea and vomiting, haemorrhage (including postpartum), burns, sepsis, heart failure, liver failure (hepatorenal syndrome), NSAIDs, ACE inhibitors and ARBs in dehydration |
| Intrinsic — tubules | Acute tubular necrosis from prolonged hypoperfusion, sepsis, aminoglycosides, contrast, herbal remedies, rhabdomyolysis, haemoglobinuria (G6PD deficiency, blackwater fever) |
| Intrinsic — interstitium | Drugs (PPIs, NSAIDs, penicillins, co-trimoxazole, rifampicin), infection |
| Intrinsic — glomeruli and vessels | Post-infectious glomerulonephritis, lupus, ANCA vasculitis, anti-GBM disease, malignant hypertension, haemolytic uraemic syndrome, pre-eclampsia and HELLP |
| Tropical causes | Severe falciparum malaria, carpet viper envenomation, leptospirosis, Lassa fever, paraquat and ethylene glycol poisoning |
| Postrenal | Prostatic enlargement or cancer, urethral stricture, bladder cancer with schistosomiasis, stones, cervical cancer obstructing both ureters, blocked catheter |
Assessment
- History — fluid losses, drugs (NSAIDs, ACE inhibitors, diuretics, antibiotics, contrast, herbal remedies), urinary symptoms, rash, joint pain or haemoptysis, snakebite, fever
- Volume status — pulse, lying and standing blood pressure, JVP, capillary refill, mucous membranes, oedema, lung crackles
- Bladder — palpable bladder; bladder scan or catheter
- Urinalysis before catheterisation
| Urine finding | Suggests |
|---|---|
| Blood and protein with red cell casts | Glomerulonephritis |
| White cells and white cell casts | Interstitial nephritis or pyelonephritis |
| Muddy brown granular casts | Acute tubular necrosis |
| Dipstick blood but no red cells on microscopy | Myoglobin or haemoglobin |
| Index | Prerenal | Acute tubular necrosis |
|---|---|---|
| Urine sodium | Below 20 mmol/L | Above 40 mmol/L |
| Fractional excretion of sodium | Below 1% | Above 2% |
| Urine osmolality | Above 500 mOsm/kg | Below 350 mOsm/kg |
These indices are unreliable after diuretics.
Bloods: urea, electrolytes, creatinine, venous gas, calcium, phosphate, full blood count and film (fragmented cells, malaria parasites), creatine kinase, liver function, CRP, blood cultures and clotting. If an intrinsic cause is suspected, add ANA, ANCA, anti-GBM, C3 and C4, serum free light chains, hepatitis B and C, HIV and a malaria test.
Imaging: renal ultrasound within 24 hours if obstruction is possible; small kidneys suggest chronic kidney disease.
Management
- Treat life-threatening problems — hyperkalaemia, severe acidosis, pulmonary oedema
- Correct volume — 250–500 mL crystalloid boluses with reassessment if dry; stop fluids and try furosemide if overloaded
- Stop or hold NSAIDs, ACE inhibitors, ARBs, diuretics (if dry), metformin, SGLT2 inhibitors, aminoglycosides; adjust drug doses for kidney function
- Treat the cause — antibiotics for sepsis; catheter or nephrostomy for obstruction; artesunate for malaria; antivenom for envenomation; generous fluids for rhabdomyolysis; immunosuppression or plasma exchange for glomerulonephritis
- Monitor — fluid balance chart, daily weight and creatinine, hourly urine output if severe
- Avoid further contrast and nephrotoxins; review nutrition
Hyperkalaemia — emergency treatment
For potassium of 6.5 mmol/L or more, or any ECG changes:
| Step | Treatment | Purpose |
|---|---|---|
| 1 | 10% calcium gluconate 10 mL IV over 2–3 minutes with cardiac monitoring; repeat if the ECG does not improve or the changes return | Protects the heart within 1–3 minutes and lasts 30–60 minutes; does not lower potassium |
| 2 | 10 units soluble insulin with 25 g glucose IV over 15 minutes | Shifts potassium into cells for 4–6 hours |
| 3 | Salbutamol 10–20 mg nebulised | Adds to the shift |
| 4 | Sodium zirconium cyclosilicate 10 g three times daily | Removes potassium through the gut |
| 5 | Dialysis if refractory | Removes potassium |
- Check glucose hourly for 6 hours after insulin, and give a 10% glucose infusion if the starting glucose was below 7 mmol/L
- Recheck potassium at 1, 2, 4, 6 and 24 hours
- Stop potassium supplements and potassium-raising drugs
Indications for dialysis
- Refractory acidosis (pH below about 7.15)
- Refractory hyperkalaemia
- Intoxication with a dialysable poison — lithium, methanol, ethylene glycol, salicylate
- Fluid overload with pulmonary oedema not responding to diuretics
- Uraemic complications — encephalopathy, pericarditis, bleeding
Where haemodialysis is costly or unavailable, acute peritoneal dialysis is an effective alternative.
Recovery
- Watch for a polyuric phase with dehydration and low potassium and sodium
- Restart ACE inhibitors and other held drugs once kidney function is stable
- Check eGFR and urine albumin at 3 months — AKI increases the risk of chronic kidney disease
Examiner questions
References
- Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, et al., eds. Harrison's Principles of Internal Medicine. 22nd ed. New York: McGraw Hill; 2025.
- Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO clinical practice guideline for acute kidney injury. Kidney International Supplements. 2012;2:1–138.