Acute renal failure due to non-traumatic rhabdomyolysis.

Abstract

Summary Seventeen patients with acute renal failure of diverse aetiology showed myoglobinuria and elevated levels of serum creatine phosphokinase (mean 119·2 Sigma u./ml) and adolase (mean 88·5 Sibley-Lehninger (SL)u./ml), indicating the presence of diffuse muscle cell injury. The primary conditions which led to rhabdomyolysis and acute renal failure were burns, eclampsia, prolonged labour, crush injury, epileptiform convulsions, status asthmaticus, viral myositis and intoxication with chemicals including copper sulphate, mercuric chloride and zinc phosphide. In 10 non-myoglobinuric patients with acute renal failure, serum creatine phosphokinase was normal (mean 8·9 Sigma u./ml) and serum aldolase was only slightly elevated (mean 11·2 SL u./ml). Although uric acid was elevated in both groups, the values were significantly higher in myoglobinuric (mean 0·728 ± 0·199 mmol/l) compared to non-myoglobinuric patients (mean 0·583 ± 0·093 mmol/l). During the oliguric phase, hypocalcaemia was observed in 82·2% of myoglobinuric patients and in 20% of non-myoglobinuric patients. Ten out of 15 patients with myoglobinuric renal failure developed hypercalcaemia during the diuretic phase whereas only 3 non-myoglobinuric patients showed a transient hypercalcaemia. Although the mean serum potassium was somewhat higher in the myoglobinuric patients, the difference between the 2 groups was not significant. It is concluded that acute renal failure associated with non-traumatic rhabdomyolysis is not infrequent and may occur in a variety of conditions where gross evidence of muscle injury is lacking.