Are parathyroidectomies still appropriate in chronic dialysis patients?

The uremic milieu generates chronic stimulatory input to the parathyroid glands, which is mediated principally by low calcium, high phosphate and low calcitriol, and results in increased parathyroid hormone (PTH) synthesis and release and an increase in parathyroid mitotic activity with the development of monoclonal areas of nodular hyperplasia. Such glands do not fully express the machinery required to mediate the suppressive inputs to the parathyroids; the extracellular calcium receptor (CaR) and the vitamin D receptor (VDR) are both downregulated. In most of these patients ablation, by parathyroidectomy or ethanol injection, provides the only means of correcting the hyperparathyroidism; apoptosis in parathyroid cells is negligible and clinically irrelevant. In practice, surgery is often delayed by a doomed and ultimately futile attempt to effect control by medical means. Better predictors of the likely success or failure of optimal non surgical management are needed. Gland size exceeding 1 cm3 and elevated PTH despite hypercalcemia (implying loss of suppressibility by calcium), in the presence of good phosphate control and adequate calcitriol provision point strongly to eventual failure of medical treatment and the need for parathyroid ablation. Parathyroidectomy, usually subtotal, remains the standard management, with ultrasound guided injection of ethanol or calcitriol showing promise in some centers. The above scenario is unlikely to be changed greatly by the new emerging vitamin D metabolites, but calcimimetic agents may well increase the scope of non surgical management.