Rhabdomyolysis is muscle breakdown with systemic consequences. The kidney is one of the major organs at risk. When skeletal muscle cells are injured, they release intracellular contents including creatine kinase, potassium, phosphate, uric acid, and myoglobin.
Myoglobin is central to rhabdomyolysis-associated kidney injury. It can contribute to tubular obstruction, direct tubular toxicity, oxidative injury, and renal vasoconstriction. Hypovolemia, acidosis, sepsis, trauma, and shock can worsen the risk of AKI. The clinical context varies.
Causes include crush injury, prolonged immobilization, seizures, severe agitation, hyperthermia, ischemia, exertion, toxins, medications, compartment syndrome, and metabolic disease. Hyperkalemia may be immediately life-threatening. Potassium is released from injured muscle cells. If renal clearance is impaired or tissue injury is ongoing, serum potassium can rise quickly and precipitate malignant dysrhythmias.