Xavier Bosch, M.D., Ph.D., Esteban Poch, M.D., Ph.D., and Josep M. Grau, M.D., Ph.D. NEJM. Volume 361:62-72 July 2, 2009 Number 1
Rhabdomyolysis — literally, the dissolution of striped (skeletal) muscle — is characterized by the leakage of muscle-cell contents, including electrolytes, myoglobin, and other sarcoplasmic proteins (e.g., creatine kinase, aldolase, lactate dehydrogenase, alanine aminotransferase, and aspartate aminotransferase) into the circulation. Massive necrosis, which is manifested as limb weakness, myalgia, swelling, and, commonly, gross pigmenturia without hematuria, is the common denominator of both traumatic and nontraumatic rhabdomyolysis.1,2 Acute kidney injury is a potential complication of severe rhabdomyolysis, regardless of whether the rhabdomyolysis is the result of trauma or some other cause, and the prognosis is substantially worse if renal failure develops. In . . .
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