Phosphate and the parathyroid

Kidney International
J Silver, T Naveh-Many

Abstract

The phosphate (Pi) retention in patients with chronic kidney disease leads to secondary hyperparathyroidism (2HPT). 2HPT is the physiological response of the parathyroid not only to Pi retention but also to decreased synthesis of 1,25(OH)(2) vitamin D, and the attendant hypocalcemia. 2HPT is characterized by increased PTH synthesis, secretion, and parathyroid cell proliferation. Extracellular fluid (ECF) Ca(2+) is recognized by the parathyroid calcium receptor and a small decrease in the ECF Ca(2+) results in relaxation of the calcium receptor and allows the unrestrained secretion and synthesis of PTH and in the longer term, parathyroid cell proliferation. Both 1,25(OH)(2) vitamin D and fibroblast growth factor 23 inhibit PTH gene expression and secretion. Secondary hyperparathyroidism can initially be controlled by a single therapeutic intervention, such as a Pi-restricted diet, a calcimimetic, or an active vitamin D analog. In this review we discuss the mechanisms whereby Pi regulates the parathyroid. Pi has a direct effect on the parathyroid which requires intact parathyroid tissue architecture. The effect of Pi, as of Ca(2+), on PTH gene expression is post-transcriptional and involves the regulated interaction of parathyroi...Continue Reading

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