Morales-Hernández AE, Pérez-Rodríguez RR, Hernández-Salcedo DR, Valencia-López R

Language: Spanish
References: 12
Page: 589-595
PDF size: 488.91 Kb.

ABSTRACT

Rhabdomyolysis is a disease characterized by skeletal muscle cell damage where intracellular toxic material is released into the systemic circulation. Among the causes are traumatic, ischemic, drug, toxic, metabolic or infectious. These causes damage to skeletal muscle cells by influencing the integrity of the plasma membrane, sarcolemma, and leads to the release of toxic material. The final pathogenic pathway is common and includes an increase in ionised free calcium in the cytoplasm. The increased cytoplasmic calcium initiates a complex network of intracellular processes, such as activation of phospholipase A2, prolonged contraction of muscle cells, mitochondrial dysfunction and production of reactive oxygen species, which eventually promote muscle cell damage and the release of various substances to the systemic circulation, leading to clinical manifestations. The pathophysiology of acute renal injury is characterized by vasoconstriction and renal ischemia accumulation of myoglobin in the distal convoluted tubule, and direct cytotoxic action of myoglobin on epithelial cells in the proximal convoluted tubules. Endothelial dysfunction and inflammation contribute to local tissue damage and organ dysfunction. The treatment for kidney failure induced by rhabdomyolysis is aggressive rehydration and may be effective for patients with a mild form of the disease. Dialysis is required in patients with severe metabolic acidosis and severe renal dysfunction related to myoglobinuria.

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