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Discussion

The initial hypocalcemia was caused by calcium binding in the necrotic muscle tissue. Once the oliguria and muscle necrosis improved, the calcium deposits were released from the tissues, resulting in hypercalcemia and PTH secretion suppression. Importantly, treatment with bisphosphonates, calcitonin, or denosumab may not be effective in lowering the calcium levels in this setting. Additionally, calcium supplementation in the hypocalcemic phase should be judicious. The predominant hypercalcemia mechanism is independent of PTH action or osteoclastic bone resorption and postulated to be caused by the dissolution of calcium precipitates. Physical removal of calcium through low calcium bath HD is indicated if aggressive hydration fails.