Acute renal failure is defined as acute oliguria (< 400 ml per day) or a rapid (hours to weeks) decline in glomerular filtration rate manifested by a rise in urea and creatinine. The rise in creatinine is often slow. In fact, if all renal function is lost, the serum creatinine rises by only 80-160 |imol litre-1 (1-2 mg dl-1) per day. Oliguria is defined as the production of 100-400 ml urine per day. Anuria is defined as the production of < 100 ml per day, whilst absolute anuria is no urine output. Absolute anuria reflects urinary tract obstruction until proven otherwise. It is generally believed that a urine output of < 0 5 ml kg-1 per hour for greater than two hours is an important marker of renal hypoperfusion and should trigger remedial action. However, 50-60% of acute renal failure is non-oliguric.
Hypotension, dehydration, and sepsis are the commonest causes of acute tubular necrosis. Prerenal causes of acute renal failure are the most common in both hospital and the community (Box 8.1). Overall mortality from unselected cases of acute renal failure has remained at around 50% (70% on ICU). Mortality increases with serum creatinine: 5-20% <165 |imol litre-1 (2 mg dl-1) and 64% over 250 |imol litre-1 (3 mg dl-1). Mortality has not changed significantly in over 20 years, making prevention of acute renal failure a high priority. Even with the advent of renal replacement therapy, the change in case mix, increasing age of patients, and severity of underlying conditions may help to explain the static mortality rate. Overall it is estimated that 5% hospital admissions and 30%
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