Abstract
Acute renal failure has oliguria and uraemia as its cardinal manifestations. The syndrome may be due to acute tubular necrosis, glomerulonephritis, urinary tract obstruction and occlusive vascular disease.
The renal damage due to acute tubular necrosis is of uncertain aetiology. Renal cortical ischaemia and depression of glomerular filtration rate are important in the pathogenesis. Activation of the renin-angiotensin system and glomerular coagulation may prove to be important in these changes.
The differentiation between reversible oliguria and established renal failure is generally accomplished on clinical grounds and the response to a therapeutic trial of mannitol. Measurement of urinary sodium concentration and osmolality are valuable adjuncts.
The keystone of management is the prevention of symptomatic uraemia. Infection and haemorrhage have now replaced pulmonary oedema and hyperkalaemia as the major causes of death. The mortality rate remains high in acute tubular necrosis and a significant mortality occurs in the diuretic phase.