Phosphate Metabolism, Hyperphosphatemia and Hypophosphatemia

Abstract

Serum phosphate level is maintained by intestinal phosphate absorption, renal phosphate handling and shift between extracellular phosphate and phosphate in bone or intracellular space. Parathyroid hormone (PTH), 1,25-dihydroxyvitamin D [1,25(OH)2D] and fibroblast growth factor 23 (FGF23) are major hormones that affect serum phosphate level by working on either kidney or intestine. PTH, 1,25(OH)2D and FGF23 work by binding to PTH1 receptor, vitamin D receptor and FGF receptor-Klotho complex, respectively. Deranged signals from these receptors cause hyperphosphatemic or hypophosphatemic diseases. In addition, there are also other causes for hyperphosphatemia and hypophosphatemia independent of the signals from these receptors. Chronic hyperphosphatemia is a risk factor for ectopic calcification including vasculature. On the other hand, chronic hypophosphatemia results in rickets/osteomalacia characterized by impaired mineralization of bone matrix. The pathogenesis and treatment of hyperphosphatemic and hypophosphatemic diseases are summarized in this paper.