Post-transplant hypercalcemia due to mobilization of metastatic calcifications. An alternative to tertiary hyperparathyroidism.

Abstract

Abstract. A case of transient hypercalcemia in a 29‐year‐old female, who received a renal transplant from her homozygotic twin‐sister, has been examined by a 47‐calcium tracer study and traditional calcium and phosphorus balance techniques. Parathyroid activity was evaluated by measuring the tubular reabsorption of calcium and the tubular maximum capacity of glucose. The study revealed a pronounced negative balance due to a pronounced hypercalcuria and a low intestinal absorption of calcium in a functionally hypoparathyroid patient. It is concluded that the hypercalcemia was caused by a mobilization of metastatic calcifications deposited in the terminal phase of uremia and during hemodialyses. It is suggested that other calcium metabolic disturbances may have a similar pathophysiological mechanism, including some cases of post‐transplant hypercalcemias, which have hitherto invariably been considered to be due to so‐called tertiary hyperparathyroidism.