Anuria and Oliguria

Oliguria is urine output below about 400 mL/day in adults, or below 0.5 mL/kg/h for 6 hours or more. Anuria is output below about 100 mL/day. Both are clinical signs of acute kidney injury, severe volume depletion, vascular compromise or urinary obstruction.

Causes

• Prerenal: hypovolaemia, haemorrhage, gastrointestinal losses, burns, low cardiac output, sepsis, hepatorenal syndrome, renal artery occlusion and drugs that reduce glomerular perfusion.
• Intrinsic renal: acute tubular necrosis, acute interstitial nephritis, glomerulonephritis, vasculitis, thrombotic microangiopathy, rhabdomyolysis, tumour lysis, myeloma cast nephropathy, cortical necrosis and cholesterol embolism.
• Postrenal: bladder outlet obstruction, bilateral ureteric obstruction, obstruction of a solitary kidney, urethral stricture, stones, tumour, retroperitoneal fibrosis and catheter blockage.
• Pseudo-oliguria: blocked, kinked or malpositioned catheter.

True anuria should prompt immediate consideration of bilateral obstruction, vascular occlusion, severe cortical necrosis or catheter failure.

• Ask about vomiting, diarrhoea, bleeding, poor intake, heart failure, liver disease, sepsis, nephrotoxic drugs, recent contrast exposure, muscle injury, lower urinary tract symptoms, haematuria, renal colic and previous renal disease.
• Assess volume status with pulse, blood pressure, jugular venous pressure, mucous membranes, oedema and lung examination.
• Look for a palpable bladder, enlarged prostate, pelvic mass and loin tenderness.
• Rash, purpura, arthralgia, livedo, blue toes and hypertension with haematuria suggest intrinsic renal disease.
• Uraemia may cause asterixis, pericardial rub, Kussmaul breathing and confusion.

Immediate danger signs are hyperkalaemia, pulmonary oedema, severe acidosis, uraemic encephalopathy or pericarditis. Haemoptysis with haematuria suggests a pulmonary-renal syndrome.

Immediate assessment

• Flush or replace the urinary catheter and perform bladder scanning when obstruction is possible.
• Record hourly urine output, daily weight and strict fluid balance.

Laboratory tests

• Creatinine, urea, potassium, bicarbonate, calcium, phosphate, urate, CK, glucose, CBC, blood film, LDH, haptoglobin, liver tests, lactate and blood gas as indicated.
• Urinalysis and microscopy for granular casts, red cell casts, white cell casts, crystals and myoglobin pattern.
• Urine sodium, urea and osmolality can support differentiation of prerenal states from tubular injury, though results are affected by diuretics and other factors.
• Autoimmune, haemolysis, paraprotein and infection studies according to clinical context.

Imaging

• Renal and bladder ultrasound urgently when obstruction is possible.
• Doppler ultrasound or CT angiography for suspected renal vascular occlusion.
• Non-contrast CT KUB for stones.
• Antegrade or retrograde studies when obstruction remains strongly suspected despite equivocal imaging.

Kidney biopsy is considered for unexplained intrinsic injury, rapidly progressive glomerulonephritis or suspected interstitial nephritis when the result will change treatment.

Immediate care

• Treat life-threatening hyperkalaemia, severe acidosis and pulmonary oedema first.
• Restore perfusion with balanced crystalloid in 250 to 500 mL boluses when hypovolaemic, reassessing frequently.
• Target mean arterial pressure around 65 mmHg or higher; use norepinephrine when shock persists despite adequate fluid resuscitation.
• Stop nephrotoxins and adjust medication doses to renal function.

Obstruction

• Bladder outlet obstruction: urethral catheter, or suprapubic catheter if urethral catheterisation fails.
• Upper tract obstruction with renal impairment, sepsis, solitary kidney or anuria: urgent ureteric stent or percutaneous nephrostomy.
• Monitor for post-obstructive diuresis and replace fluid and electrolyte losses appropriately.

Hyperkalaemia

• Calcium gluconate 10% 10 to 30 mL IV for ECG changes.
• Soluble insulin 10 units IV with 25 g glucose, with prolonged glucose monitoring.
• Salbutamol 10 to 20 mg nebulised.
• Sodium bicarbonate when significant metabolic acidosis is present.
• Potassium removal with loop diuretics if producing urine, potassium binders, or dialysis when refractory.

Other treatment

• Use loop diuretics for fluid overload, not to force renal recovery.
• Treat sepsis promptly with appropriate antibiotics and source control.
• Rhabdomyolysis: isotonic crystalloid, electrolyte management and avoidance of nephrotoxins.
• Hepatorenal syndrome: albumin plus vasoconstrictor therapy such as terlipressin or norepinephrine and transplant evaluation.
• Glomerulonephritis and vasculitis: immunosuppression according to cause.
• Thrombotic microangiopathy, tumour lysis, myeloma and renal vascular thrombosis need cause-specific urgent therapy.

Renal replacement therapy

• Indications include refractory hyperkalaemia, severe acidosis, refractory pulmonary oedema, uraemic pericarditis or encephalopathy and dialysable toxins.
• Continuous therapy is preferred in marked haemodynamic instability or raised intracranial pressure.

Monitor urine output, renal function and electrolytes closely through the recovery phase and reassess renal function and blood pressure after discharge because acute kidney injury increases future chronic kidney disease risk.