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Calcium metabolism in acute renal failure due to rhabdomyolysis.
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1993
Year
Electrolyte DisorderRenal PathologyParathyroid DiseaseMuscle Calcium DepositsOsteoporosisParathyroid HormoneElectrolyte DisturbanceAcute Kidney InjuryChronic Kidney DiseaseMineral MetabolismHealth SciencesHemodialysisAcute Renal FailureSodium HomeostasisKidney FailureRenal PathophysiologyDiuretic ResistanceCase ReportUrologyPhysiologyMetabolismMedicineNephrology
We report a patient with drug and hyperthermia induced rhabdomyolysis who developed acute renal failure. During the oliguric phase of 22 days, there was profound hypocalcemia (lowest ionized calcium of 0.34 mmol/l), associated with appropriately elevated intact PTH levels and high normal 1,25(OH)2D levels. Massive calcification in necrotic muscle occurred during this time. In the recovery phase, hypercalcemia was present lasting 33 days (maximum ionized calcium of 1.99 mmol/L), associated with suppression of PTH secretion, low 1,25(OH)2D3 levels, decreased bone resorption and mobilization of the muscle calcium deposits. This case report illustrates that the changes in serum calcium in rhabdomyolysis-associated acute renal failure are explicable by the deposition or removal of mineral into or from necrotic muscle with the parathyroid and vitamin D changes occurring secondarily.