Regresar

Rhabdomyolysis: Molecular bases and clinical presentations

Abstract:

Rhabdomyolisis is defined as the death of striated muscle fibers, a phenomenon that may occur in response to various causes, including myocyte energy depletion, physical cell injury, direct myotoxicity by drugs, toxins and infectious and inflammatory processes; drugs of abuse, hydroelectrolytic and endocrine disorders. Despite the widely heterogeneous etiologies, the molecular mechanisms underlying rhabdomyolysis tend to converge in dysregulation of intracellular calcium metabolism –which is essential for muscle contraction–, leading to activation of lipases and proteases, mitochondrial dysfunction and oxidative stress, finalizing in myocyte death. Rhabdomyolysis is accompanied by a broadly variable clinical syndrome characterized by electrolytic disorders, elevated serum creatine kinase, and especially acute kidney injury due to the nephrotoxic effect exerted by myoglobin released from destroyed myocytes. This review describes the pathophysiologic pathways observed during rhabdomyolisis and its impact on renal function.