Calcium metabolism in acute renal failure due to rhabdomyolysis.
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.
Hadjis
T
T
Medical Intensive Care Unit, Montreal General Hospital, McGill University, Quebec, Canada.
Grieff
M
M
Lockhat
D
D
Kaye
M
M
D058186:Acute Kidney Injury / Q000209:etiology* / Q000378:metabolism; D000328:Adult; D002114:Calcinosis / Q000209:etiology; D002118:Calcium / Q000378:metabolism*; D003891:Desipramine / Q000506:poisoning; D004100:Dihydroxycholecalciferols / Q000378:metabolism; D005260:Female; D006801:Humans; D006934:Hypercalcemia / Q000209:etiology; D006996:Hypocalcemia / Q000209:etiology; D009132:Muscles / Q000378:metabolism / Q000473:pathology; D010281:Parathyroid Hormone / Q000378:metabolism; D012206:Rhabdomyolysis / Q000139:chemically induced / Q000150:complications* / Q000378:metabolism
D004100:Dihydroxycholecalciferols; D010281:Parathyroid Hormone; D002118:Calcium; D003891:Desipramine