If normal calcium is unable to be maintained by intestinal calcium absorption, or if 1,25(OH)2D is inappropriately high, then both 1,25(OH)2D and PTH, acting via their receptors, release calcium bone and increase reabsorption of calcium from the distal tubule of the kidney, resulting in hypercalcemia–hypercalciuria and possible nephrocalcinosis [84]. Here, PTH is linked to nephrocalcinosis.