Early intervention in acute renal failure

Oliguria and a rise in the plasma urea concentration are normal physiological responses to the haemodynamic changes associated with hypovolaemia, cardiac failure, or sepsis. Clinical decision making during the ensuing hours may determine whether a patient makes a speedy recovery or develops the serious complication of established acute renal failure. This condition still has a mortality of about 50%, despite recent improvements in clinical practice.¹ A meta-analysis in this week's BMJ by Ho and Sheridan reviews the evidence on one commonly used and cheap intervention—the loop diuretic furosemide (frusemide)—but finds it to be of little use in preventing or treating acute renal failure.²

Acute renal failure occurs in a variety of different circumstances and can complicate pre-existing chronic renal failure. The traditional split into prerenal, renal, and postrenal causes of acute failure is useful, if only to remind doctors of the need for a systematic approach to diagnosis and management of the underlying cause. It is appropriate that prerenal causes come first, because the treatment of hypovolaemia to maintain renal perfusion is the only reliable means of renal protection,³ and intravenous fluids will probably need to be tried for most patients. This includes elderly patients, in whom comorbidity may complicate the picture, and patients with oedema, who may none the less have depletion of intravascular fluids.

Typically, junior members of the medical staff are responsible for the initial management of these patients. These doctors need early induction into a method of rapid clinical assessment, such as the acute life threatening emergencies: recognition and treatment (ALERT) course.⁴ Doctors should take a pragmatic and prompt approach to intravenous fluid replacement, based on the patient's blood pressure, capillary refill time, and venous filling. They must watch out for and treat life threatening complications, such as hyperkalaemia, and catheterise the patient to measure the volume of urine hourly.

If the patient remains oliguric after correction of hypovolaemia, the next step is to distinguish between intrinsic renal pathology and obstructive causes. Acute renal failure may be the result of obstruction of the urinary tract, particularly in patients with only one functioning kidney. While total anuria suggests obstruction, the presence of oliguria or even polyuria does not exclude it.⁵

An ultrasound examination of the renal tract is warranted, mainly to identify obstructive changes and also to measure the bipolar length of the kidneys. Small kidneys suggest chronic renal disease. Ultrasound examination can be misleading, however, and additional imaging may be required.⁶ Obstruction should be identified promptly so that it can be treated with urinary catheterisation, ureteric stenting, or nephrostomy. Delay can result in permanent but avoidable renal injury.

The immediate cause of acute renal failure may seem obvious, but contributory factors such as nephrotoxic drugs, metabolic disturbance (including hypercalcaemia, hyperuricaemia, and paraproteinaemia), and occult sepsis should not be overlooked. Epidemics of acute renal failure may follow outbreaks of haemolytic uraemic syndrome associated with diarrhoea, and other infections such as malaria and leptospirosis may cause renal failure by diverse mechanisms.

The more common causes in any location may change over time, as was noted in one unit in the United Kingdom between 1956 and 1988, when a relative reduction in acute renal failure due to obstetric and traumatic causes and an increase in cases in elderly patients with complicated medical and surgical conditions were seen.⁷ When the cause of acute renal failure is not obvious, medical teams must consider unusual or rare explanations—such as allergic interstitial nephritis, acute glomerulonephritis, and vasculitis—conditions that require urgent assessment by a specialist and aggressive treatment.

Renal specialists are not necessary, however, for patients to receive continuous renal replacement therapy by pumped venovenous haemofiltration systems.⁸ Continuous renal replacement allows prompt initiation of treatment at the earliest stages of renal dysfunction by anaesthetic staff in the intensive therapy unit. Patients with acute renal failure tend to fall under the care of either nephrologists or anaesthetists, and this split has made it hard to conduct clinical trials during the early stages of the illness.

The meta-analysis by Ho and Sheridan in this issue is therefore timely, and provides a valuable assessment of the role of loop diuretics in the prevention and treatment of acute renal failure.² The use of loop diuretics has a theoretical basis and some support from animal studies, but the evidence from clinical studies is not strong. The results of the meta-analysis show that furosemide has no clinical benefit in the prevention or treatment of established acute renal failure.

In normal practice many clinicians, including nephrologists, think that furosemide may help increase urine output in acute renal failure, ease the management of fluid balance, and reduce the degree of hyperkalaemia.⁹ The evidence from Ho and Sheridan's paper—that furosemide does not improve mortality, does not reduce the need for renal replacement therapy or the number of dialysis sessions required, and may increase the risk of ototoxicity—must temper this opinion. The priorities in treating acute renal failure are to optimise fluid balance, treat underlying causes, and initiate renal replacement therapy at the appropriate time.