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 diur etic recovery phase after rhabdomyolysis. The pathophysiology of the h ypercalcemia observed in the recovery phase is a subject of debate. Se veral mechanisms have been proposed, including mobilization of calcium from muscle deposits, secondary hyperparathyroidism, and elevated lev els of 1,25 dihydroxyvitamin D. The authors report the case of a 30-ye ar-old man admitted for evaluation of marked hypercalcemia (18.3 mg/dL ) who was hospitalized 3 weeks earlier for acute renal failure seconda ry to rhabdomyolysis. Plasma parathyroid hormone and 1,25 dihydroxyvit amin D levels were suppressed during the period of maximal hypercalcem ia. A technetium pyrophosphate scan demonstrated extensive deposition of calcium throughout the pelvic and lower extremity muscles. This cas e of delayed hypercalcemia after rhabdomyolysis supports the hypothesi s that mobilization of calcium deposits from soft tissue, including mu scle, is central to the pathogenesis of this syndrome.