Case report: delayed hypercalcemia after rhabdomyolysis-induced acute renal failure.

Abnormal calcium metabolism is a common complication of rhabdomyolysis -induced acute renal failure. During the oliguric phase, patients are frequently hypocalcemic. Hyperphosphatemia and skeletal resistance to parathyroid hormone are believed to be possible underlying mechanisms. In addition, there have been reports of hypercalcemia during the diuretic recovery phase after rhabdomyolysis. The pathophysiology of the hypercalcemia observed in the recovery phase is a subject of debate. Several mechanisms have been proposed, including mobilization of calcium from muscle deposits, secondary hyperparathyroidism, and elevated levels of 1,25 dihydroxyvitamin D. The authors report the case of a 30-year-old man admitted for evaluation of marked hypercalcemia (18.3 mg/dL) who was hospitalized 3 weeks earlier for acute renal failure secondary to rhabdomyolysis. Plasma parathyroid hormone and 1,25 dihydroxyvitamin D levels were suppressed during the period of maximal hypercalcemia. A technetium pyrophosphate scan demonstrated extensive deposition of calcium throughout the pelvic and lower extremity muscles. This case of delayed hypercalcemia after rhabdomyolysis supports the hypothesis that mobilization of calcium deposits from soft tissue, including muscle, is central to the pathogenesis of this syndrome.