Published in:
Open Access 01-12-2016 | Case report
Sudden onset of parathyroid hormone-independent severe hypercalcemia from reversal of tumoral calcinosis in a dialysis patient
Published in: BMC Nephrology | Issue 1/2016
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Background
Tumoral calcinosis is a rare manifestation of extraskeletal calcification, featuring large calcified cystic masses in the periarticular regions of large joints. In chronic kidney disease (CKD), this disorder is thought to evolve through a chronically elevated calcium-phosphorus solubility product leading to calcium precipitation in soft tissue. Treating tumoral calcinosis in these patients involves interventions to lower the calcium-phosphorus product such as reduction in vitamin D therapy and intensive hemodialysis regimens.
Case Presentation
We report the case of a 54-year old woman with polycystic kidney disease on peritoneal dialysis with widespread tumoral calcinosis in the context of hypercalcemic tertiary hyperparathyroidism who had been on long-term alfacalcidol therapy. After withdrawal of the vitamin D analogue and initiation of daily hemodialysis, there was rapid dissolution of her tumoral calcium deposits with the abrupt onset of parathyroid hormone (PTH)-independent transient hypercalcemia that resolved once the soft tissue deposits disappeared.
Conclusions
Resorption of soft tissue calcific deposits may result in transient parathyroid hormone (PTH)-independent hypercalcemia. In CKD patients, this hypercalcemia causes a decrease in the PTH level, distinguishing it from tertiary hyperparathyroidism, though PTH may not be totally suppressed, the way it is seen in PTH-independent hypercalcemia in non-CKD patients.