A transient elevation of serum creatinine disproportionate to the elevation of blood urea nitrogen (BUN) is common in early acute rhabdomyolysis. Presumably, this results from release of creatine from injured muscle, which is spontaneously dehydrated to creatinine. The usual ratio of urea nitrogen to creatinine in serum is 10:1. Ratios of 5 or less shortly after onset suggest acute rhabdomyolysis. Uric acid in serum may exceed 40 mg/dL. Purines released from injured muscle are converted to urate in the liver. Hyperuricemia of this magnitude is seldom seen in other conditions, even acute tumor lysis induced by chemotherapy. Leukocytosis is common in rhabdomyolysis of any etiology. Hypoalbuminemia, especially when associated with hemoconcentration, is an ominous sign and implies major capillary damage with leakage of plasma components out of the vascular space. On rare occasions, capillary damage may be so extensive that erythrocytes also escape into interstitial tissues. This results in shock with an acute reduction of hematocrit in the absence of bleeding or hemolysis. In oliguric patients, a urine sodium concentration above 20 mEq/L suggests tubular injury. However, the urine sodium concentration may be low in cases of myoglobinuria and, accordingly, this finding in pigment nephropathy may be less helpful than in other oliguric settings. Hyperkalemia is often observed as a consequence of release of potassium from damaged muscle cells. Profound hypocalcemia, with serum calcium values below 3.0 mg/dL, may result from hyperphosphatemia and trapping of calcium in injured muscle. Hypercalcemia may occur later, especially during the diuretic phase of acute renal failure. Usually, this is seen in patients who have been given calcium salts earlier in the illness.