ACUTE RENAL FAILURE DEFINITION Acute renal failure is characterized by a rapid decrease of glomerular filtration and, in consequence, reduced clearance of products of metabolism and other substances. This is usually accompanied by oliguria or anuria, but sometimes polyuria, with a progressive rise of serum creatinine and blood urea nitrogen (BUN), electrolyte imbalance and the development of metabolic acidosis. TOXIC CAUSES Aminoglycosides (e.g.: gentamycin, kanamycin). Carbon tetrachloride Polymycin Ethylene glycol Heavy metals Myoglobin and haemoglobin NON-TOXIC CAUSES May be classified as pre-renal, renal and post-renal in origin. The principal causes are: Acute tubular necrosis Acute glomerulonephritis Renal artery obstruction Acute interstitial nephritis Obstructive uropathy CLINICAL FEATURES The main sign is oliguria or anuria, occurring over several hours or a few days. Sometimes, however, renal failure occurs without oliguria, with normal or increased excretion of water and electrolytes. Accompanying signs and symptoms of acute renal failure include: weakness, apathy, loss of appetite, nausea, vomiting, increasing metabolic acidosis, deep, frequent respiration (Kussmaul type), pulmonary oedema, peripheral oedema, ascites, and coma. Cardiac dysrhythmia and extreme muscular weakness may be due to electrolyte imbalance (hyperkalaemia, hypercalcaemia). DIFFERENTIAL DIAGNOSIS Acute urinary retention Pre-renal uraemia (dehydration, hypotension). RELEVANT INVESTIGATIONS Biochemically, acute renal failure is characterized by elevated blood urea concentration and an increasing serum creatinine concentration. Serum potassium concentration usually rises above 6.5 mmol/L. Arterial blood gases indicate metabolic acidosis. The ECG may be helpful to assess hyperkalaemia. TREATMENT Carefully monitor clinical condition, ideally in a specialized ward. Control fluid balance and serum electrolyte levels, especially hyperkalaemia and hyponatremia. Correct contributing factors such as hypovolaemia and hypertension. Stop exposure to the offending agent(s). Carefully monitor dosage of potentially nephrotoxic drugs, if they are absolutely necessary. Administer furosemide in doses of 250 mg (up to 1 g/day) intravenously; in children, 2 to 5 mg/kg (up to 15 mg/kg/ day). Start dopamine in continuous intravenous infusion (up to 3 µg/kg/minute). Control fluid intake. Control calorie intake. Hemodialysis or peritoneal dialysis should be instituted urgently in the following instances: a. Hyperkalaemia with cardiac dysrrhythmias; b. Hyperhydration in the anuric patient c. Refractory metabolic acidosis. CLINICAL COURSE AND MONITORING Monitor fluid balance, electrolytes, cardiac status, acid-base balance, and infections. Particular care should be taken with fluid balance during the polyuric phase. Most patients recover. Renal function should be monitored until normalized. LONG-TERM COMPLICATIONS Chronic renal dysfunction. AUTHOR(S)/PEER REVIEW Author: Dr. C. Bismuth, HÔpital Fernand Widal, Paris, France. Peer Review: Cardiff, March 1995. Berlin, October 1995: V. Danel, T. Meredith, J. Szajewski, A. Wong, J. Pronczuk.