ORE CURRICULUM IN NEPHROLOGY Disorders of Calcium, Phosphorus, and Magnesium

arathyroid hormone (PTH) ● Released in response to lowering of ionized Ca via Ca-sensing receptor inactivation (ionized Ca decreases PTH release) ● Cleaved from pre-pro PTH to pro PTH to PTH in gland, and then secreted and catabolized to N-terminal (active) and C-terminal fragments. Most of the C-terminal fragments are inactive, but some C-terminal fragments (sometimes called “7-84” fragments although true sequence is not known) may have antagonistic effects on bone via different receptors. ● Activity: Increases Ca reabsorption (and decreases P reabsorption) from kidney Increases bone resorption by multiple mechanisms Indirectly increases intestinal absorption by enhancing conversion of 25(OH) vitamin D to 1,25(OH) vitamin D ● Regulation: Hypocalcemia stimulates PTH secretion Calcitriol (1,25[OH]2D) inhibits PTH secretion, and PTH increases conversion of vitamin D to calcitriol, thereby completing feedback loop for regulation Hyperphosphatemia stimulates PTH secretion Severe hypomagnesemia stimulates PTH secretion