Hypercalcemia Complicated by Rhabdomyolysis and Acute Kidney Injury

Rhabdomyolysis is a condition resulting from muscle breakdown due to trauma, extreme exertion, or seizures, causing the release of intracellular contents including potassium and phosphate (Pi). Abnormalities in serum calcium (Ca) levels have also been reported in rhabdomyolysis, although its exact mechanism remains controversial. A 57-year-old male was admitted due to tonic-clonic seizures caused by epilepsy. On the second day of hospitalization, he exhibited high creatine phosphokinase (CPK) levels (39,253 U/L) and elevated serum creatinine (Cr) levels (2.31 mg/dL), indicating rhabdomyolysis and acute kidney injury (AKI). Because of anuria and azotemia, he started hemodialysis from the third day. Subsequently, renal function gradually improved, and he was weaned off hemodialysis. However, around the 20th day of hospitalization, serum Ca levels began to rise, reaching a peak of 13.3 mg/dL. A computed tomography (CT) scan showed calcification in the left-side muscles including the pectoralis major and upper arm, and bone scintigraphy also demonstrated a high accumulation of technetium-99m hydroxymethylene diphosphonate (^99mTc-HMDP) in the same areas. Treatment with denosumab was administered for hypercalcemia, and serum Ca levels returned to normal. On the 45th day, a follow-up CT scan showed the disappearance of the calcific deposits, and no accumulation was seen in the bone scintigraphy.