Rhabdomyolysis (literally dissolution of striated muscle) is myonecrosis on a massive scale with leakage of myofiber contents, including myoglobin, CK, and other proteins into the circulation. Myonecrosis is caused by two basic mechanisms, mechanical physical injury and energy depletion. Failure of ATP-powered pumps allows influx of calcium into the myofiber. Calcium activates proteases and phospolipases, leading to disintegration of plasma membrane, contractile filaments, and other myofiber contents.
The causes of rhabdomyolysis are listed in the table below.

Clinically, rhabdomyolysis is characterized by weakness, myalgia, and muscle swelling, and biochemically by elevation of CK, which is proportionate to the extent of myonecrosis. Muscle regenerates rapidly following myonecrosis. The most important complication of severe rhabdomyolysis is renal failure. When plasma myoglobin exceeds 0.5-1.5 mg/dl, it leaks into the urine and when its urine concentration rises above 100 mg/dl, it gives urine a red-brown color  (myoglobinuria) and precipitates in distal tubules in the form of casts. Myoglobinuria is used synonymously with rhabdomyolysis. A large proportion of acute renal failure cases and associated deaths are caused by rhabdomyolysis. Myoglobin causes intrarenal vasoconstriction, tubular injury, and tubular obstruction by casts.

Further reading
Bosch X, Poch E, Grau JM. Rhabdomyolysis and Acute Kidney Injury. N Engl J Med 2009;361:62-72 PubMed

Updated: July, 2009