GANGGUAN GINJAL AKUT AKIBAT RHABDOMIOLISIS

Abstract

Acute kidney injury (AKI) is the most serious complication of rhabdomyolysis, a syndrome characterized by skeletal muscle destruction causing leakage of myoglobin and other intracellular protein as well as electrolytes into circulation. Due to its light molecular weight, myoglobin is readily filtered by the glomerus, and enters renal tubules, which may cause acute kidney injury with myoglobinuria. It is also characterized by significant increase of serum creatine kinase (CK) as well as electrolyte abnormalities. This review is intended to elucidate the mechanisms involved in pathogenesis of rhabdomyolysis induced AKI, which is related with its clinical as well as laboratory manifestations. This is used as a basis to determine correct diagnosis and management.The basic mechanisms in the pathogenesis of rhabdomyolysis induced AKI include: 1) renal vasoconstriction and ischemia induced by the release of several mediators which promote vasoconstriction including endothelin-1 and vasopressin which is triggered by activation of sympathetic system and rennin angiotensin aldosteron (RAA) system to compensate hypovolemia. Additionally TNF-α, thromboxane A 2 , and F 2 Isoprostane are also generated in inflammatory response to muscle injury, endothelial dysfunction as well as oxidative injury, 2) formation of myoglobin cast, which is precipitation of myoglobin-Tamm Horsfal protein complex producing obstruction of distal tubules, 3) direct cytotoxic effect of myoglobin on proximal tubules through oxidative injury generated by Fenton Reaction and myoglobin redox cycling. It is concluded that rhabdomyolysis induced AKI is produced by renal ischemia, tubular obstruction and oxidative injury on tubular cells.