Oliguria

The pathological processes involved are either pre-renal, renal or post-renal. Pre-renal problems account for approximately 70% of outpatient cases of ARF and up to 60% of hospital-based cases.¹ Oliguria is rarely found in chronic renal failure.

• Pre-renal causes include:
  • Dehydration
  • Vascular collapse
  • Low cardiac output
• Renal problems are associated with structural renal damage e.g. acute tubular necrosis, primary glomerular diseases or vascular lesions.
• Post-renal failure is secondary to a mechanical or functional obstruction to the flow of urine. The commonest cause is a blocked catheter.² This usually responds to release of the obstruction.

• Excessive fluid loss e.g. diarrhoea, vomiting.
• Drug use e.g. gentamicin, non-steroidal anti-inflammatories.
• 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 e.g. 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.²

• There may be signs due to ARF e.g. oedema, anaemia.
• Signs of congestive heart failure e.g. gallop rhythm and hepatomegaly.
• Hypertension may be present.
• Signs of the underlying disease e.g. a butterfly rash on the face and joint swelling suggest systemic lupus erythematosus.

• MSU dipstick:
  • In prerenal failure:
    • There are few hyaline and fine granular casts are observed.
    • There is little protein, haem or red cells.
  • In intrinsic renal failure:
    • 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 e.g. CRP in sepsis.
• Urinary electrolytes and serum electrolytes should be monitored:
  • Urinary electrolytes are valuable indicators of functioning renal tubules.
  • The fractional excretion of sodium (FENa) may be a useful indicator. However nonoliguric 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 prerenal 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:
  • In prerenal failure:
    • The ratio of urinary to plasma creatinine is high- > 40.
    • The urinary sodium concentration is low - < 20 mEq/L.
  • In intrinsic renal failure the findings are opposite.
• Full blood count - anaemia results from dilution and decreased erythropoiesis.
• Arterial blood gases - for acid-base status and pA O₂.
• Renal ultrasound with doppler.
• Initially kidney biopsy is not necessary. If prerenal and postrenal 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 mEq/L .
• Potassium administration is contraindicated 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 currently 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 e.g. 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.

Renal failure that results from nephrotoxic injury, interstitial nephritis and neonatal asphyxia is frequently of the nonoliguric type. It is related to a less severe renal injury and has a better prognosis.

Mortality rates in oliguric ARF vary according to the underlying cause and associated medical condition. It may be 5% for patients with community-acquired ARF, 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 e.g. hypertension, congestive heart failure and pulmonary oedema.
• Gastrointestinal e.g. anorexia, nausea, vomiting and ileus.
• Haematological e.g. 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.