Acute Renal Failure

Acute renal failure means abrupt deterioration in parenchymal renal function which is usually, but not invariably, reversible over a period of days or weeks. In clinical practice, such deterioration in renal function is sufficiently severe to result in uraemia. Oliguria is usually, but not invariably, a feature. Acute renal failure may cause sudden, life-threatening biochemical disturbances and is a medical emergency. The distinction between acute and chronic renal failure may not be readily apparent in a patient presenting with uraemia. Patients with chronic renal impairment are not immune from the development of a superimposed acute-on-chronic renal failure under appropriate circumstances.

Renal failure results in reduced excretion of nitrogenous waste products of which urea is the most commonly measured. A raised serum urea concentration (uraemia) may conveniently be classified as: (i) prerenal, (ii) renal or (iii) postrenal. More than one category may be present in an individual patient.

The term 'renal failure' means failure of renal excretory function owing to depression of the glomerular filtration rate. This is accompanied to a variable extent by failure of erythropoietin production, vitamin D hydroxylation, regulation of acid-base balance and regulation of salt and water balance and blood pressure.

Course and prognosis of Acute Renal Failure

The clinical course of acute renal failure associated with ATN is variable depending on the severity and duration of the renal insult. Oliguria is common in the early stages: non-oliguric renal failure is usually a result of a less severe renal insult. Recovery of renal function typically occurs after 7-21 days, although recovery is delayed by continuing sepsis. In the recovery phase, GFR may remain low while urine output increases, sometimes to many litres a day owing to defective tubular reabsorption of filtrate.

The clinical course is variable and ATN may last for up to 6 weeks even after a relatively short-lived initial insult. Eventually renal function usually returns almost to normal or to normal, although exceptions exist (e.g. in renal cortical necrosis - see below). During the recovery phase the kidneys appear relatively insensitive to further insult, such as a recurrence of hypovolaemia.

Treatment of Acute Renal Failure

No treatment is, as yet, known which will reduce the duration of acute renal tubular necrosis once it has occurred. Claims that intravenous mannitol, furosemide (frusemide) or 'renal-dose' dopamine may do so are not supported by controlled trial evidence, and none of these treatments is without risk.

No overall benefit has been proven from the use of the synthetic analogue of atrial natriuretic factor, anaritide, in reducing the duration of or mortality from ATN. However, oliguric patients did appear to do better whilst non-oliguric ones did worse when treated with this agent in a large clinical trial.