of calcium are given in Table 2. The homeostatic control of this narrow concentration range of Pi is maintained by several hormones, including PTH, 1,25(OH)2 vitamin D, calcitonin, insulin, glucagon, and others, but the control is never as rigorous as that of serum calcium. In contrast to calcium balance, which is primarily regulated in the small intestine by 1,25(OH)2 vitamin D, Pi balance is mainly regulated by the phosphaturic effect of PTH on the kidney, primarily the proximal convoluted tubule. In this sense, Pi regulation is less critical than that of calcium, which may result from the presence of multiple stores of this ion distributed throughout the body (i.e., bone, blood, and intracel-lular compartments).

A major regulator of Pi is PTH, whose role has been fairly well uncovered. PTH increases bone resorption of Pi (and calcium ions), it blocks renal tubular Pi reabsorption following glomerular filtration (whereas PTH favors calcium reabsorption), and it enhances intestinal Pi absorption (and calcium absorption) via the vitamin D hormone, 1,25(OH)2 vitamin D. Other hormones have more modest effects on serum Pi concentration.

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