Acute oligo-anuria

At a glance

• Oliguria is urine output under 0.5 mL/kg/hour for 6 hours (KDIGO stage 1 by urine output) or under about 400 mL/day. Anuria is under 100 mL/day.
• Oliguria often precedes a rise in creatinine by a day or more. In hospital it is frequently the earliest sign of AKI.
• Exclude obstruction first: flush the catheter, scan the bladder. Total anuria is obstruction until proven otherwise.
• Then sort the cause as pre-renal, intrinsic renal or post-renal, treat it, and look for an urgent indication for dialysis.
• KDIGO 2012 still defines and stages AKI. KDIGO's 2026 AKI and acute kidney disease (AKD) update, which adds structural biomarkers to the definition, has completed public review; the final version had not been published at the time of writing.

Causes

Category	Typical causes	Clues
Pre-renal	Hypovolaemia (bleeding, vomiting, diarrhoea, burns, over-diuresis), sepsis, cardiogenic shock, cirrhosis with hepatorenal physiology, ACE inhibitor or ARB plus NSAID in a volume-depleted patient	Low BP, postural drop, low JVP or clear heart failure; bland urine; FENa under 1%
Intrinsic: tubular	ATN from prolonged hypoperfusion, sepsis, contrast, aminoglycosides, vancomycin, rhabdomyolysis	Granular "muddy brown" casts, urine sodium over 40 mmol/L
Intrinsic: glomerular	RPGN (ANCA, anti-GBM, lupus), post-infectious GN	Blood and protein on dipstick, red cell casts, rash, haemoptysis
Intrinsic: interstitial	Drug AIN (PPIs, penicillins, NSAIDs, immune checkpoint inhibitors), pyelonephritis	White cells and white cell casts, sometimes rash and eosinophilia
Intrinsic: vascular	Renal artery occlusion or dissection, renal vein thrombosis, cholesterol emboli, TMA, scleroderma renal crisis	Flank pain and high LDH (infarct), livedo after angiography, haemolysis and low platelets
Post-renal	Prostatic enlargement, clot retention, blocked catheter, bilateral ureteric stones or tumour, retroperitoneal fibrosis, pelvic malignancy	Palpable bladder, anuria or fluctuating output, hydronephrosis

• Abdominal compartment syndrome is a cause in ICU after major abdominal surgery or massive resuscitation: bladder pressure over 20 mmHg with new organ dysfunction.
• Post-renal AKI needs obstruction of both kidneys, of a single functioning kidney (including a transplant), or of the bladder outlet.

Pitfall: fluctuating output, or anuria alternating with polyuria, suggests intermittent obstruction.

Focused history

• Volume losses and intake, recent surgery, fluid balance charts and weights.
• Drugs: ACE inhibitors, ARBs, diuretics, NSAIDs, SGLT2 inhibitors, metformin, aminoglycosides, vancomycin with piperacillin-tazobactam, contrast in the past 72 hours.
• Urinary symptoms: hesitancy, poor stream, frank haematuria with clots, flank pain.
• Systemic features: rash, arthralgia, haemoptysis, sinus symptoms, weight loss (vasculitis, lupus, myeloma).
• Muscle injury: a long lie, crush, seizures, statins, heat illness.
• Recent angiography or vascular surgery (cholesterol emboli), known AF (renal infarct), cancer or pelvic radiotherapy (obstruction).

Focused examination

• Volume status: HR, BP including postural, JVP, capillary refill, skin turgor, oedema, lung bases. One clinical sign is unreliable; combine them.
• Palpable bladder and a prostate examination if retention is possible.
• Signs of sepsis, liver disease, heart failure.
• Skin: purpura (vasculitis), livedo reticularis and blue toes (cholesterol emboli), malar rash.
• Muscle tenderness or compartment tension (rhabdomyolysis).

Red flags

These need action within hours:

• Total anuria: obstruction, vascular occlusion or RPGN.
• Potassium 6.5 mmol/L or more, or ECG changes. See Hyperkalaemia.
• Pulmonary oedema with falling output.
• Severe acidosis (pH under 7.15).
• Fever with obstruction (pyonephrosis): needs drainage, not just antibiotics.
• Haematuria and proteinuria with rising creatinine: possible RPGN. See Rapidly progressive glomerulonephritis.

Investigations

• Bedside: bladder scan or catheter flush, hourly urine output via catheter in the unwell patient, ECG.
• Bloods: creatinine and urea (compare with baseline), electrolytes, venous gas, FBC and film, CK, LFTs, calcium, phosphate, urate, LDH.
• Urine dipstick before a catheter if possible (catheter trauma causes haematuria), then microscopy and urine sodium, creatinine, and albumin- or protein-creatinine ratio.
• Renal tract ultrasound: within 24 hours if obstruction is possible and the cause is unclear, within 6 hours if pyonephrosis is suspected (NICE NG148). Small kidneys suggest chronic disease.
• Targeted tests: ANCA, anti-GBM, ANA, complement, serum free light chains and protein electrophoresis, blood cultures, haptoglobin.

Urine indices

Index	Pre-renal	ATN
Urine sodium	Under 20 mmol/L	Over 40 mmol/L
FENa	Under 1%	Over 2%
FE urea (useful on diuretics)	Under 35%	Over 50%
Urine osmolality	Over 500 mOsm/kg	Under 350 mOsm/kg
Sediment	Bland or hyaline casts	Muddy brown granular casts

• FENa = (urine Na × plasma creatinine) ÷ (plasma Na × urine creatinine) × 100. Keep the creatinine units the same.
• Pitfall: FENa is low in several intrinsic causes: contrast nephropathy, rhabdomyolysis, early obstruction, acute GN and hepatorenal syndrome. It is high after diuretics and in CKD. Interpret it with the whole picture.

Management

Immediate

1. Relieve obstruction: catheter for bladder outlet obstruction; nephrostomy or ureteric stent for upper tract obstruction. An obstructed infected kidney is a urological emergency.
2. Assess volume and perfuse: if hypovolaemic, give a crystalloid bolus of 250 to 500 mL (balanced crystalloid such as Plasma-Lyte or Hartmann's in most) and reassess. Target MAP of 65 mmHg or more in septic shock, using noradrenaline if needed.
3. Stop or hold nephrotoxins (NSAIDs, aminoglycosides, IV contrast where avoidable) and the drugs on the UK-derived "sick day" list, SADMANS: sulfonylureas, ACE inhibitors, diuretics (unless overloaded), metformin, ARBs, NSAIDs and SGLT2 inhibitors.
4. Dose-adjust renally cleared drugs: low molecular weight heparin, gabapentinoids, opioids such as morphine, antibiotics.
5. Treat the cause: sepsis, bleeding, cardiac failure, rhabdomyolysis (aggressive fluids to urine output 200 to 300 mL/hour if tolerated).

Pitfall: repeated fluid boluses to "push" urine output in a euvolaemic patient with ATN cause pulmonary oedema. A positive fluid balance independently predicts death in critically ill AKI.

Diuretics

• Loop diuretics don't prevent or treat AKI. Use them only for fluid overload.
• The furosemide stress test (1 mg/kg IV, or 1.5 mg/kg if previously exposed) has prognostic value: urine output under 200 mL over 2 hours predicts progression to stage 3 and need for KRT.

Indications for urgent kidney replacement therapy

Indication	Threshold
Hyperkalaemia	K⁺ 6.5 mmol/L or more, or ECG changes, despite medical treatment
Acidosis	pH under 7.15 with a metabolic cause, refractory to treatment
Fluid overload	Pulmonary oedema not responding to diuretics
Uraemic complications	Pericarditis, encephalopathy, bleeding
Toxins	Dialysable drugs: lithium, toxic alcohols, metformin-associated lactic acidosis, salicylates

• STARRT-AKI (NEJM 2020, about 3,000 ICU patients): accelerated KRT in severe AKI without an urgent indication didn't reduce 90-day mortality and left more survivors dialysis-dependent.
• AKIKI 2 (Lancet 2021): once patients reached oliguria over 72 hours or urea over 40 mmol/L, delaying further until an urgent indication gave no benefit in KRT-free days. 60-day mortality was 55% versus 44% (p=0.07), significant only in an adjusted secondary analysis (HR 1.65, 95% CI 1.09 to 2.50), which the authors read as potential harm.
• In practice: start KRT for an urgent indication, and reassess daily whether one is approaching. Continuous KRT is usual in haemodynamically unstable ICU patients.

After relief of obstruction

• Post-obstructive diuresis (commonly defined as output over 200 mL/hour for 2 consecutive hours, or over 3 L in 24 hours) can follow catheterisation of chronic retention. Monitor output hourly, electrolytes 6- to 12-hourly, and replace losses partly (for example, half to two-thirds of output) rather than chase every millilitre.

Follow-up

• Review creatinine within 3 months after AKI. An episode of AKI raises the risk of CKD, cardiovascular events and further AKI.
• Restart held drugs (ACE inhibitor, SGLT2 inhibitor, metformin) once creatinine is stable and the patient is eating and drinking. Write the plan in the discharge summary.

Special situations

• Older people: less reserve, and a "normal" creatinine may hide low GFR. Retention from anticholinergics or opioids is common.
• Pregnancy: consider pre-eclampsia, HELLP, acute fatty liver of pregnancy and obstructed ureters from the gravid uterus. Mild hydronephrosis is normal in pregnancy, especially on the right.
• Transplant kidney: anuria needs urgent graft ultrasound with Doppler to exclude arterial or venous thrombosis and obstruction. See Fever in renal transplant recipients.
• Aboriginal and Torres Strait Islander people have higher rates of CKD, so acute-on-chronic disease is common. Remote patients may need early retrieval because dialysis isn't available locally.

Pitfalls

• Checking the catheter last instead of first.
• Calling oliguria "pre-renal" on clinical impression and giving litres of fluid without reassessing volume status.
• Reading FENa without considering diuretics, contrast or rhabdomyolysis.
• Forgetting urine microscopy. Red cell casts change the diagnosis and the urgency.
• Missing a single functioning kidney: unilateral obstruction then causes anuria.
• Starting dialysis on a creatinine number alone, rather than on a complication or its trajectory.