Ls. Sperling et Ja. Tumlin, CASE-REPORT - DELAYED HYPERCALCEMIA AFTER RHABDOMYOLYSIS-INDUCED ACUTE-RENAL-FAILURE, The American journal of the medical sciences, 311(4), 1996, pp. 186-188
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.