Rhabdomyolysis is characterized by skeletal muscle necrosis resulting in release of large amounts of toxic muscle cell components, including electrolytes, myoglobin, and other sarcoplasmic proteins into circulation. Creatinine phosphokinase (CPK) and myoglobin serum levels constitute the diagnostic hallmark. Nowadays, drugs have become one of the most frequent cause of rhabdomyolysis and acute kidney injury (AKI) is a potential life-threatening complication. The mechanisms involved in the development of AKI in rhabdomyolysis are intrarenal vasoconstriction, direct and ischemic tubule injury and tubular obstruction. According to some clinical series, the mortality rate in patients who develop AKI due to rhabdomyolysis is highly variable. The cornerstone in managing this condition is the early, aggressive repletion of fluids. The composition of replacement fluid remains controversial. Saline and sodium bicarbonate, especially in patients with metabolic acidosis, seem to be a reasonable approach. When AKI produces refractory hyperkalemia, acidosis or volume overload, renal replacement therapy is indicated.