Renal failure occurs in approximately 10 per cent of patients, unless the cause is acetaminophen (paracetamol) poisoning when the incidence is very much higher, approaching 75 per cent in patients with grade IV encephalopathy. The mechanism in this circumstance is a direct nephrotoxic effect of acetaminophen. In patients without acetaminophen poisoning, many factors may contribute to the pathogenesis of renal failure. The usual form of renal failure is the hepatorenal syndrome, characterized by a progressive increase in plasma creatinine concentration, oliguria, low urine sodium concentration (usually < 10 mmol/l), and histologically normal kidneys. Acute tubular necrosis may also occur as a result of hypotension, hypovolemia, or severe sepsis. It may be difficult to differentiate between these two syndromes, and often a diagnosis of hepatorenal syndrome can only be made after correction of the predisposing causes for acute tubular necrosis. Management includes monitoring of volume status, volume loading (although clearly this must be balanced against the risk of worsening cerebral edema), and optimization of hemodynamic status. Low-dose dopamine is commonly used to promote diuresis but, as in other conditions, its benefits are unproven. If renal failure develops, early dialysis is indicated. Continuous techniques of dialysis are preferred because of greater hemodynamic stability and consequent benefits to the intracranial pressure. Even if renal replacement therapy is required, survival can be as high as 30 to 50 per cent, depending upon the etiology.
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