Oliguria

oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

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.[1]

The pathological processes involved are either pre-renal, renal or post-renal. Pre-renal problems account for approximately 70% of outpatient cases of acute kidney injury (AKI) and up to 60% of hospital-based cases.[1] Oliguria is rarely found in chronic kidney disease.

  • Pre-renal causes include:
  • 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.[2] This usually responds to release of the obstruction.

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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.[2]

  • Mid-stream specimen of urine (MSU) dipstick:
    • Prerenal:
      • There are few hyaline and fine granular casts.
      • There is little protein, haemoglobin or red cells.
    • In intrinsic acute kidney injury (AKI):
  • 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.[3]
    • 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.
  • Treatment of any reversible causes.[4]
  • 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 acute kidney injury (AKI).
    • There also seems to be no difference in outcome between the use of intermittent haemodialysis and continuous renal replacement therapy (CRRT), but this is under investigation.[5][6]
    • 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:[7]
      • 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.

Surgical

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.

Acute kidney injury (AKI) that 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. It may be 5% for patients with community-acquired AKI, but as high as 80% in multi-organ failure patients in intensive care.[1]

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.

Further reading & references

  • Kellum JA; Acute kidney injury. Crit Care Med. 2008 Apr;36(4 Suppl):S141-5.
  1. Devarajan P; Oliguria, eMedicine, Dec 2008
  2. Oliguria tutorial, Student BMJ; July 1999
  3. Agraharkar M et al, Acute Renal Failure, eMedicine, Jan 2011
  4. Klahr S, Miller SB; Acute oliguria. N Engl J Med. 1998 Mar 5;338(10):671-5.
  5. Gibney N, Cerda J, Davenport A, et al; Volume management by renal replacement therapy in acute kidney injury. Int J Artif Organs. 2008 Feb;31(2):145-55.
  6. 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.
  7. Mantel GD; Care of the critically ill parturient: oliguria and renal failure. Best Pract Res Clin Obstet Gynaecol. 2001 Aug;15(4):563-81.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Hayley Willacy
Current Version:
Last Checked:
18/03/2011
Document ID:
1707 (v22)
© EMIS