A structured bedside approach to the cause: pre-renal, intrinsic, post-renal, with urine tests, ultrasound and the furosemide stress test.
At the bedside
- 1
History and drug chart
Hypotension, sepsis, vomiting/diarrhoea, contrast, NSAIDs, ACEi/ARB, diuretics, aminoglycosides, vancomycin + piperacillin-tazobactam, colistin, amphotericin, herbal/indigenous medicines, snakebite, rhabdomyolysis risk.
- 2
Assess volume and perfusion
MAP, CRT, lactate, JVP/CVP, lung B-lines, IVC, fluid balance; venous congestion (high CVP) also reduces GFR.
- 3
Exclude obstruction
< 24 hBladder scan / catheter flush; renal ultrasound for hydronephrosis, kidney size (small = CKD), stones.
- 4
Urine tests
Dipstick (blood/protein), microscopy (muddy brown casts = ATN; RBC casts = GN; WBC casts/eosinophils = AIN), urine Na/FeNa (< 1% suggests pre-renal if not on diuretics), FeUrea < 35% if on diuretics, urine protein:creatinine.
- 5
Bloods
Creatinine, urea, K, bicarbonate/ABG, Ca, PO4, CK (rhabdo), LDH and smear (haemolysis, TMA), platelets, LFT, cultures. Serology if GN suspected: ANA, ANCA, anti-GBM, C3/C4, hepatitis B/C, HIV.
- 6
Furosemide stress test (optional)
2 hEuvolaemic, stage 1-2 AKI: furosemide 1 mg/kg IV (1.5 mg/kg if exposed); urine < 200 mL in 2 h predicts progression to stage 3/RRT.
- 7
Refer for biopsy/nephrology
Active sediment, nephrotic-range proteinuria, unexplained AKI, suspected vasculitis/TMA or AIN.
Furosemide stress test
Furosemide
- Dose
- 1 mg/kg (1.5 mg/kg if on loop diuretics)
- Worked example
- 70 kg diuretic-naive: 70 mg IV; replace urine output mL-for-mL with crystalloid if needed; < 200 mL in 2 h = high risk
Only in euvolaemic patients.
Causes of AKI in Indian ICUs
| Category | Common causes |
|---|---|
| Pre-renal / haemodynamic | Sepsis, hypovolaemia (diarrhoea, vomiting, bleeding), cardiorenal, hepatorenal, ACEi/NSAIDs |
| Intrinsic - tubular | Ischaemic/septic ATN, contrast, aminoglycosides, colistin, rhabdomyolysis, haemolysis (G6PD, malaria), snakebite |
| Intrinsic - interstitial | Drug-induced AIN (PPIs, beta-lactams), leptospirosis, pyelonephritis |
| Intrinsic - glomerular/vascular | Post-infectious GN, lupus, vasculitis, HUS/TTP, malignant hypertension |
| Post-renal | BPH, stones, cervical/prostate cancer, blocked catheter |
Calculators for this topic
References
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Finding the cause of AKI
Step 1 of ~3
Decision: Obstruction on bladder scan/ultrasound?
Based on Kidney Disease: Improving Global Outcomes (KDIGO) AKI Work Group. Educational use; follow local protocol.
Pathophysiology
Pre-renal states cause avid sodium and water retention (low urine Na, FeNa < 1%), which reverses quickly with restored perfusion. Prolonged insult leads to tubular injury with loss of concentrating ability (urine Na > 40, FeNa > 2%, muddy brown casts).
Evidence
- Chawla 2013: furosemide stress test urine < 200 mL in 2 h had AUC 0.87 for progression to stage 3 [Chawla 2013].
- KDIGO 2012 recommends evaluating cause in all AKI and avoiding diuretics to prevent or treat AKI except for fluid overload [KDIGO 2012].
Controversies
- FeNa is unreliable in sepsis, contrast nephropathy and CKD.
🇮🇳 India notes
- Ask specifically about indigenous medicines (some contain heavy metals or aristolochic acid), hair dye (paraphenylenediamine) ingestion, and snakebite.
- Leptospirosis AKI is typically non-oliguric with hypokalaemia; Russell's viper AKI often needs RRT.
References
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Test yourself
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Educational reference for trained clinicians. Check doses against your hospital protocol and the patient in front of you.