BACKGROUND: In a third of patients presenting with rhabdomyolysis-induced acute renal failure (ARF), a biphasic plasma calcium profile may occur. METHODS: We report a case of rhabdomyolysis-induced ARF presenting hypocalcemia during oliguria, followed by a severe hypercalcemia in the polyuric phase. A hypocalcemia-induced acute increase of plasma parathyroid hormone in the early stage of ARF was followed by a down-regulation of parathyroid hormone, 1,25(OH)2 vitamin D and 25(OH) vitamin D during the renal function recovery, associated with an acute hypercalcemia. The plasma calcium increase induced in our patient severe neurological disturbances, life-threatening short QT interval and Brugada-like syndrome at risk of malignant arrhythmias. This complication was treated by hemodialysis and pamidronic acid infusion. RESULTS: This case confirms that the pathogenesis of the biphasic calcium profile may be related to the massive calcium uptake in the ischemic muscle cells during oliguria, followed by a muscle calcium release later in the polyuric stage of ARF. Therefore, the behavior of calciotropic hormones may be the consequence rather than the cause of plasma calcium changes. CONCLUSIONS: We would like to emphasize the danger of sudden death that may occur in the recovery phase of rhabdomyolysis-induced ARF when the physician might be wrongly convinced that the major risks have disappeared.
BACKGROUND: In a third of patients presenting with rhabdomyolysis-induced acute renal failure (ARF), a biphasic plasma calcium profile may occur. METHODS: We report a case of rhabdomyolysis-induced ARF presenting hypocalcemia during oliguria, followed by a severe hypercalcemia in the polyuric phase. A hypocalcemia-induced acute increase of plasma parathyroid hormone in the early stage of ARF was followed by a down-regulation of parathyroid hormone, 1,25(OH)2 vitamin D and 25(OH) vitamin D during the renal function recovery, associated with an acute hypercalcemia. The plasma calcium increase induced in our patient severe neurological disturbances, life-threatening short QT interval and Brugada-like syndrome at risk of malignant arrhythmias. This complication was treated by hemodialysis and pamidronic acid infusion. RESULTS: This case confirms that the pathogenesis of the biphasic calcium profile may be related to the massive calcium uptake in the ischemic muscle cells during oliguria, followed by a muscle calcium release later in the polyuric stage of ARF. Therefore, the behavior of calciotropic hormones may be the consequence rather than the cause of plasma calcium changes. CONCLUSIONS: We would like to emphasize the danger of sudden death that may occur in the recovery phase of rhabdomyolysis-induced ARF when the physician might be wrongly convinced that the major risks have disappeared.