THE ROLE OF THE PARATHYROID-GLANDS IN THE UREMIC SYNDROME

The genesis of hyperparathyroidism in uremia has turned out to be quit e complex, involving low calcitriol, low ionized calcium, and possibly direct effects of high phosphate as well as the action of local facto rs and modifier genes determining the hyperplastic response of the gla nd. Growth is initially polyclonal and later monoclonal. In addition, the response of target tissues to parathyroid hormone (PTH) is attenua ted (''PTH resistance''), and this may be due, at least in part, to di minished phenotypic expression of PTH receptors. In a series of elegan t studies, it has been shown that PTH acts not only on the classical t arget organs of calcium homeostasis (ie, bone and kidney), but also on nonclassical. The role of PTH excess in the genesis of several featur es of the uremic syndrome, for example muscle dysfunction, cardiomyopa thy, leukocyte and T-cell dysfunction or insulin secretion by pancreat ic islet cells, has been established. These studies have borne out the prediction that PTH is a ''uremic toxin.'' (C) 1995 by the National K idney Foundation, Inc.