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.