Acute renal failure is an abrupt decrease in renal function sufficient to result in azotaemia—retention of nitrogenous waste in the body. (79) Acute renal failure can result from a decrease of renal blood flow (prerenal azotaemia), intrinsic renal disease (renal azotaemia), or obstruction of urine flow (postrenal azotaemia). Prerenal azotaemia can be caused by renal arterial occlusion or a decrease in the effective blood volume (e.g. haemorrhage, fluid pooling, congestive heart failure, diarrhoea, massive diuresis). Intrinsic renal azotaemia is most commonly caused by acute tubular necrosis due to an acute ischaemic or nephrotoxic insult. Less commonly, renal azotaemia is caused by vasculitis, acute postinfectious glomerulonephritis, or drug-induced acute interstitial nephritis. Postrenal azotaemia is due to obstruction of the urine collecting system, as occurs with bladder outlet obstruction, bilateral ureteral obstruction, or ureteral obstruction in a solitary kidney.
Medical complications of acute renal failure include hyperkalaemia, hyperuricaemia, arrhythmias, anaemia, coagulopathies, vomiting, nausea, and urinary tract infections. The main neuropsychiatric manifestations include somnolence, delirium, asterixis (flapping tremor), neuromuscular irritability, and seizures. (80> Mental status abnormalities in acute (but not chronic) renal failure begin to occur for most adults when the serum creatinine level acutely rises to about 4.0 mg/dl. In oliguric renal failure, serum blood urea nitrogen levels can be expected to rise by about 10 to 20 mg/dl per day. Serum creatinine levels can be expected to rise about 1 mg/dl per day. Neuropsychiatric complications of acute renal failure are best treated by correcting the underlying cause of the renal failure. Dialysis may be used to manage acute manifestations. While awaiting reversal of neuropsychiatric manifestations, symptomatic management with antiseizure medications and neuroleptics may be necessary.
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