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Oliguria is defined as passing a reduced urine volume. It is a clinical characteristic of acute kidney injury (AKI). Oliguria is defined as a urine output that is:

  • Less than 1 mL/kg/hour in infants.
  • Less than 0.5 mL/kg/hour in children.
  • Less than 400 mL/day in adults.

The pathological processes involved are either pre-renal, renal or post-renal. Pre-renal problems account for approximately 70% of outpatient cases of AKI and up to 60% of hospital-based cases. Intensive care unit and surgical patients are at increased risk of AKI and oliguria.[1]Oliguria is rarely found in chronic kidney disease.

  • Pre-renal causes include:
    • Dehydration
    • Vascular collapse
    • Low cardiac output
  • Renal problems are associated with structural renal damage - eg, acute tubular necrosis, primary glomerular diseases or vascular lesions.
  • Post-renal causes are any mechanical or functional obstruction to the flow of urine. The most common cause is a blocked catheter. This usually responds to release of the obstruction.
  • Excessive fluid loss - eg, diarrhoea, vomiting.
  • Drug use - eg, gentamicin, non-steroidal anti-inflammatory drugs.
  • Children may give a history of gross haematuria and oedema suggesting glomerular disease. Previous streptococcal infection may suggest a postinfectious glomerulonephritis. A history of bloody diarrhoea may precede the haemolytic uraemic syndrome.
  • Symptoms of urinary tract obstruction - eg, complete failure to pass urine. This is ANURIA; it is a medical emergency and should be investigated with an ultrasound scan, arranged urgently.

Findings will vary according to the cause. The patient may be very unwell - extremely breathless, pale, clammy and shut down peripherally with an unrecordable blood pressure.

  • There may be signs due to AKI - eg, oedema, anaemia.
  • Signs of congestive heart failure - eg, gallop rhythm and hepatomegaly.
  • Hypertension may be present.
  • Signs of the underlying disease - eg, a butterfly rash on the face and joint swelling suggest systemic lupus erythematosus.
  • Midstream specimen of urine (MSU) dipstick:
    • Prerenal:
      • There are few hyaline and fine granular casts.
      • There is little protein, haemoglobin or red cells.
    • In intrinsic AKI:
      • Haematuria and proteinuria are prominent.
      • Broad brown granular casts are found in ischaemic or toxic acute tubular necrosis.
      • Red cell casts are usually observed in acute glomerulonephritis. The urine in acute interstitial nephritis has white cells.
  • Other tests may be indicated by underlying cause - eg, C-reactive protein (CRP) in sepsis.
  • Renal function, urinary electrolytes and serum electrolytes (sodium and potassium) should be monitored:
    • Urinary electrolytes are valuable indicators of functioning renal tubules.
    • The fractional excretion of sodium (FENa), which is the percentage of sodium filtered by the kidney, which is excreted in the urine, may be a useful indicator. However, non-oliguric patients, those with glomerulonephritis or those receiving diuretics may have misleading results.
    • The formula for calculating the FENa is as follows:
      • FENa = (UrinaryNa/PlasmaNa)/(UrinaryCr/PlasmaCr) x 100.
      • In patients with pre-renal condition, the FENa is usually less than 1%.
      • With intrinsic conditions, the FENa is greater than 1%.
      • Exceptions to this rule are problems caused by radiocontrast nephropathy, severe burns, acute glomerulonephritis and rhabdomyolysis.
    • In patients who are receiving diuretics, a fractional excretion of urea (FEUrea) is used because urea transport is not affected by diuretics.
    • The formula for calculating the FEUrea is as follows:
      • FEUrea = (Uurea/Purea)/(UCr/PCr) x 100.
      • FEUrea of less than 35% is suggestive of a pre-renal condition.
  • Serum creatinine:
    • Pre-renal:
      • The ratio of urinary to plasma creatinine is high (>40).
      • The urinary sodium concentration is low (<20 mmol/L).
    • In intrinsic AKI, the findings are opposite.
  • FBC - anaemia results from dilution and decreased erythropoiesis.
  • Arterial blood gases - for acid-base status and pAO2.
  • Renal ultrasound with Doppler.
  • Initially kidney biopsy is not necessary. If pre-renal and post-renal causes have been ruled out and an intrinsic renal disease is suspected, renal biopsy may be valuable in establishing diagnosis.

Early recognition of AKI may improve outcome.[2]

  • Treatment of any reversible causes.
  • Restoration of intravascular volume.
  • Strict fluid balance and correction of electrolyte abnormality.
  • Input and output records, daily weights, physical examination and serum sodium are used to determine ongoing therapy.
  • Emergency treatment of hyperkalaemia is indicated when serum potassium exceeds 6.5 mmol/L.
  • Potassium administration is contra-indicated until urine flow is established.
  • Dialysis:
    • There is some controversy regarding the timing of dialysis, as it may delay the recovery of patients with an AKI.
    • There also seems to be no difference in outcome between the use of intermittent haemodialysis and continuous renal replacement therapy (CRRT); however, this is under investigation.[3, 4]
    • Although not frequently used, peritoneal dialysis can also technically be used in acute cases and probably is tolerated better haemodynamically than conventional haemodialysis.
    • Indications for dialysis in patients with AKI are as follows:
      • Volume expansion that cannot be managed with diuretics.
      • Hyperkalaemia refractory to medical therapy.
      • Uraemia.
    • Dialysis may be required until the kidneys recover:[5]
      • The general goal of dialysis is to remove endogenous and exogenous toxins and to maintain the fluid, electrolyte and acid-base balance.
      • There are no absolute indications for acute dialysis. The decision depends on the onset, duration and severity of the abnormality to be corrected.


Patients with oliguria secondary to obstruction, frequently require urological surgery - eg, nephrostomy. Percutaneous nephrostomy is a simple technique for temporary drainage of an obstructed kidney. Under local anaesthesia, a ureteric catheter is passed through a needle into the renal pelvis and is connected to a drainage bag.

AKI which results from nephrotoxic injury, interstitial nephritis and neonatal asphyxia is frequently of the non-oliguric type. It is related to a less severe renal injury and has a better prognosis.

Mortality rates in oliguric AKI vary according to the underlying cause and associated medical condition.[6]The most common causes of death are sepsis, heart and lung failure and withdrawal of life support.

  • Cardiovascular complications because of fluid and sodium retention - eg, hypertension, congestive heart failure and pulmonary oedema.
  • Gastrointestinal - eg, anorexia, nausea, vomiting and ileus.
  • Haematological - eg, anaemia and platelet dysfunction.
  • Hyperkalaemia produces ECG abnormalities and arrhythmias.
  • Infections; there may be impaired immunity secondary to uraemia.
  • Neurological complications include confusion, sleepiness and seizures.

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Further reading and references

  1. Godin M, Bouchard J, Mehta RL; Fluid balance in patients with acute kidney injury: emerging concepts. Nephron Clin Pract. 2013123(3-4):238-45. doi: 10.1159/000354713. Epub 2013 Sep 4.

  2. Gonzalez F, Vincent F; Biomarkers for acute kidney injury in critically ill patients. Minerva Anestesiol. 2012 Dec78(12):1394-403. Epub 2012 Oct 2.

  3. Gibney N, Cerda J, Davenport A, et al; Volume management by renal replacement therapy in acute kidney injury. Int J Artif Organs. 2008 Feb31(2):145-55.

  4. Ghahramani N, Shadrou S, Hollenbeak C; A systematic review of continuous renal replacement therapy and intermittent haemodialysis in management of patients with acute renal failure. Nephrology (Carlton). 2008 Jun 1.

  5. Mantel GD; Care of the critically ill parturient: oliguria and renal failure. Best Pract Res Clin Obstet Gynaecol. 2001 Aug15(4):563-81.

  6. Kellum JA; Acute kidney injury. Crit Care Med. 2008 Apr36(4 Suppl):S141-5.