Discuss pathophysiology of acute renal failure in rhabdomyolysis.
The myoglobin released during rhabdomyolysis can lead to direct tubular toxicity by obstructing the renal tubules and causing cell injury. The heme moiety of myoglobin can also lead to oxidative stress and lipid peroxidation, which can further damage the renal tubular cells. Ad
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The release of creatine kinase during rhabdomyolysis can also contribute to acute renal failure. Elevated levels of creatine kinase can cause vasoconstriction and reduce renal blood flow, leading to ischemic injury. In addition, the breakdown of creatine kinase can lead to the production of adenosine, which can cause vasoconstriction and further reduce renal blood flow.
The release of potassium during rhabdomyolysis can also contribute to acute renal failure. Hyperkalemia can cause cardiac arrhythmias, which can lead to reduced cardiac output and decreased renal perfusion. Hyperkalemia can also cause direct toxicity to the renal tubular cells, leading to renal injury.
Overall, the pathophysiology of acute renal failure in rhabdomyolysis is complex and multifactorial, involving direct tubular toxicity, oxidative stress, vasoconstriction, ischemic injury, and electrolyte imbalances. Treatment typically involves aggressive hydration and electrolyte management, along with measures to prevent further muscle breakdown and promote renal recovery.