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Phosphorus is a critical element in skeletal development, bone mineralization, membrane composition, nucleotide structure, and cellular signaling. Similar to calcium, the serum phosphorus level is maintained within a narrow range through a complex interplay between intestinal absorption, exchange with intracellular and bone storage pools, and renal tubular reabsorption. The principal organ that regulates phosphate homeostasis is the kidney. Hypophosphatemia stimulates 1,25-dihydroxyvitamin D (calcitriol) synthesis via the 25(OH)D-1α-hydroxylase in the kidney, leading to increased calcium and phosphorus absorption in the intestine and enhanced mobilization of calcium and phosphorus from bone. In addition, hypophosphatemia is a potent stimulator of an increase in maximal tubular reabsorption of phosphate. The resulting increased serum calcium inhibits PTH secretion with a subsequent increase in urinary calcium excretion and an increased tubular reabsorption of phosphate. Thus, normal serum calcium levels are maintained and serum phosphorus levels are returned to normal. PTH regulates phosphate reabsorption, but its principal function is to maintain calcium homeostasis. PTH increases urinary phosphate excretion through reduced expression of the type IIa sodium-phosphate transporter. This effect is rapid and is achieved by internalization of the transporter from the brush border membrane and enhanced lysosomal degradation (1).

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