Rhabdomyolysis is the breakdown of skeletal muscle fibers with release of intracellular contents—myoglobin, creatine kinase (CK), potassium, phosphorus, uric acid, and lactate dehydrogenase—into the circulation. The muscle cell membrane (sarcolemma) is disrupted when intracellular calcium rises uncontrollably due to ATP depletion (ischemic causes) or direct membrane injury (traumatic/toxic causes). Elevated intracellular calcium activates proteases, lipases, and phospholipases that destroy the cell from within. The released myoglobin is freely filtered by the glomerulus, but in the acidic environment of the renal tubules, myoglobin precipitates into casts that obstruct tubular flow. Myoglobin also generates reactive oxygen species through its iron (Fe2+) moiety, causing direct tubular epithelial cell injury via lipid peroxidation. The combination of tubular obstruction, direct cytotoxicity, and renal vasoconstriction (from nitric oxide scavenging by free myoglobin) causes acute kidney injury (AKI) in 15-33% of cases. Additionally, massive potassium release can cause life-threatening hyperkalemia and cardiac arrhythmias, while calcium-phosphorus product elevation can cause hypocalcemia and metastatic calcification.