Rhabdomyolysis and myohemoglobinuric acute renal failure.

Muscle accounts for approximately 40% of total body mass and falls victim to a wide variety of toxic, ischemic, infectious, inflammatoiy, and metabolic insults. The final result of these diverse assaults may be muscle fiber dissolution, or rhabdomyolysis, resulting in the release of potentially toxic intracellular components into the systemic circulation. The rhabdomyolysis syndrome has been recognized for centuries. Indeed, the Bible alludes to its occurrence [1]. However, it was not until Bywaters' and Beall's classic description of the "crush syndrome," a result of the bombing raids of London during World War II, that the renal complications of rhabdomyolysis became firmly entrenched in the medical literature [2]. Since then, a plethora of non-traumatic causes of muscle necrosis have been recognized, and today rhabdomyolysis is considered a leading cause of acute renal failure (ARF). For example, at Harborview Medical Center, a Seattle municipal hospital, it accounts for approximately 10 to 15% of all ARF cases. In recent years, a number of important pathophysiologic insights into the nature of rhabdomyolysisinduced ARF have emerged, offering potentially new prophylactic and therapeutic approaches. Therefore, this article has the following goals: (1) review the pathophysiology of myonecrosis, in general, and some of its specific causes; (2) discuss how muscle necrosis can negatively impact the kidney, potentially culminating in tubular necrosis and ARF; and (3) using this pathophysiologic information as a backdrop, review current and possible future pharmacologic approaches for the management of this dramatic and often life threatening "myo-renal syndrome."