Research Center for Trauma in Police Operations, Directorate of Health, Rescue & Treatment, Police Headquarter, Tehran, Iran

Skeletal muscle damage in rhabdomyolysis can cause the release of the contents of damaged myocytes into the bloodstream and acute kidney damage as a serious complication. In this syndrome, the levels of serum creatine kinase and urine myoglobin increase significantly. Better knowledge of the pathophysiology of rhabdomyolysis and its resulting acute kidney damage can help maintain kidney function by increasing treatment options.

This review study focuses on epidemiology, pathophysiology, causes, effective mechanisms, diagnosis, and management of acute renal injury following rhabdomyolysis. Any form of muscle injury can cause rhabdomyolysis. Ageing, trauma, drug abuse, and infections have been identified as the most common causes of rhabdomyolysis.

Paying attention to the underlying pathology and effective mechanisms in the incidence of acute renal injury following rhabdomyolysis can play a key role in measuring the severity of injury, triage, and treatment of patients. Also, the study of biological findings can play a key role in identifying rhabdomyolysis patients at risk of acute kidney injury, predicting different stages of injury, reducing mortality and morbidity, and improving treatment protocols.

Rhabdomyolysis has been introduced as an important clinical challenge. Non-specific symptoms, presence of multiple causes for its onset, and systemic problems in patients complicate diagnosis and treatment. Understanding the pathology of myoglobin-induced acute kidney injury and extensive fluid therapy are the cornerstones of treatment. All physicians should be aware of the common causes, diagnosis, and treatment options because one of the most important treatment goals in these conditions is to avoid acute kidney damage.