Tertiary Hyperparathyroidism After Renal Transplantation

Demineralization of bone begins early in chronic renal failure, probably as a result of defective calcium absorption associated with disordered metabolism of vitamin D.¹ Hyperphosphatemia and metabolic acidosis also contribute, albeit in a lesser degree, to the calcium deficit. Persistent hypocalcemia subsequently provokes compensatory parathyroid hyperplasia, with resulting generalized osteitis and metastatic calcification of soft tissue. And the hyperplasia may persist even after renal failure has been rectified by a transplanted kidney. This autonomous hyperfunctioning of the parathyriod gland, often referred to as tertiary or autonomous hyperparathyroidism, continues to produce skeletal demineralization and osteitis despite restored normal renal function, and the resulting disability may become severe enough to necessitate surgical removal of the hyperplastic gland.

How frequent is tertiary hyperparathyroidism and how often is surgery required for its correction? Clearly, it is difficult to find answers to these questions in studies on uremic patients who did not receive a