We studied six oliguric patients with rhabdomyolysis-induced acute renal failure. On admission, all had marked hyperphosphatemia and hypocalcemia associated with low levels of 1,25-dihydroxycholecalciferol [1,25(OH)2D]. During the early polyuric phase, moderate hypercalcemia was accompanied by marked elevations in plasma 1,25(OH)2D and persistent elevations in parathyroid hormone (both amino and carboxy terminals). During the late polyuric phase, the levels of serum calcium and 1,25(OH)2D reverted to normal. Thus, in rhabdomyolysis-induced acute renal failure, the hypocalcemia of the oliguric phase may be secondary to decreased synthesis of 1,25(OH)2D; severe hyperphosphatemia may also have a major role. The hypercalcemia of the polyuric phase may be partly due to increased synthesis of 1,25(OH)2D, resulting from the high parathyroid hormone levels and recovery of renal function. (N Engl J Med. 1981; 305:117–23.) RHABDOMYOLYSIS-induced acute renal failure is being diagnosed with increasing frequency.1 2 3 It is commonly associated with drug or alcohol overdose, and it is characterized by severe muscle necrosis and deterioration of renal function. Biochemical features of this disorder that are not usually seen in renal failure due to other causes include marked elevation of various muscle enzymes in association with profound hyperphosphatemia and hyperuricemia. Abnormalities in calcium metabolism are frequent in rhabdomyolysis-induced acute renal failure.1 2 3 Marked hypocalcemia in the oliguric phase and moderate hypercalcemia in the early polyuric phase have been reported.2 3 4 Hyperphosphatemia and skeletal resistance to the calcemic action of.
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