Figure 111

The recent discovery of the calcium-sensing receptor and increased understanding of its expression along the nephron have provided explanations for many of the known effects of hypercalcemia to cause clinical disturbances in renal tubular function [1]. In the parathyroid gland the calcium-sensing receptor allows the cell to sense extracellular levels of calcium and transduce that signal to regulate parathyroid hormone production and release. In the nephron, expression of the calcium receptor can be detected on the apical surface of cells of the papillary collecting duct, where calcium inhibits antidiuretic hormone action. Thus, hypercalcemia impairs urinary concentration and leads to isotonic polyuria. The most intense expression of the calcium receptor is in the thick ascending limb of the loop of Henle, particularly the cortical portion, where the calcium receptor protein is located on the basolateral side of the cells; this explains the known effects of hypercalcemia in inhibiting reabsorption of calcium, magnesium, and sodium chloride in the thick ascending limb [2]. In addition, hypercalcemia causes hypercalciuria through an increased filtered calcium load and suppression of parathyroid hormone release with a consequent reduction in calcium reabsorption. Ca—calcium; Mg—magnesium; NaCl—sodium chloride.

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