Crush syndrome (systemic manifestations of traumatic rhabdomyolysis) is the second leading cause of death after earthquakes or other destructive disasters. Crush-related acute kidney injury (AKI) is the most important Component of crush syndrome, and medical professionals living in disaster-prone regions should know about its pathophysiology, clinical and laboratory features, complications, and treatment. Pathogenesis of AKI on the basis of crush injuries is multifaceted. The most important mechanism is compartment syndrome-related hypovolemia, and consequent renal hypoperfusion, which may result in ischemic acute tubular necrosis. Also, rhabdomyolysis-related myoglobinuria may result in the formation of kidney-damaging myoglobin casts and direct tubular toxicity. Formation of uric acid plugs, oxidant injury, increased serum levels of cytokines, and still many other factors may take a role in the pathogenesis as well. Crush syndrome can cause serious electrolyte imbalances, sepsis, and bleeding, which can further exacerbate AKI. Early recognition and appropriate management, which includes aggressive hydration and management of electrolyte imbalances can help to prevent or minimize kidney damage. This review provides an overview of the pathophysiology, complications, and treatment of AKI in the context of Crush syndrome.