[Secondary hyperparathyroidism in patients with renal failure.]

In renal failure, several factors lead to parathyroid gland overactivity, manifested by hypersecretion of parathyroid hormnone (PTH) and glanudal hyperplasia eventually leading to monoclonal expansion of glandular cells in severe cases. Main factors contributing to this secondary hyperparathyoidism are increased end-organ resistance to PTH, low serum calcium and high serum phosphate concentrations and decreased production of 1,25-dihydroxyvitamin D3 by the kidneys. Treatment is directed towards correction of these underlying disturbances in meneral metabolism, however, such maneuvers are not always successful in controlling parathyroid gland activity. Functional disturbances within the parathyroid glands e.g., decrements in vitamin D or calcium sensing receptor number or function and/or increased cell mass have been implicated in therapeutic resistance. This article discusses the role of such functional derangements and details the results of a recent study demonstrating the importance of gland mass in this context.