The causes of hypo- and hyperphosphatemia in humans

Koumakis, Eugénie<sup>1</sup>; Cormier, Catherine<sup>1</sup>; Roux, Christian<sup>1</sup>; Briot, Karine<sup>1</sup>

Affiliations

¹Reference Center for Rare Disorders of Calcium and Phosphate Metabolism, Reference Center for Rare Genetic Bone Disorders, OSCAR Filière, Rheumatology Department, Cochin Hospital, AP-HP Centre-Paris University, 27 Rue du Faubourg Saint-Jacques, 75014 Paris, France

Abstract and keywords

Phosphate homeostasis involves several major organs that are the skeleton, the intestine, the kidney, and parathyroid glands. Major regulators of phosphate homeostasis are parathormone, fibroblast growth factor 23, 1,25-dihydroxyvitamin D, which respond to variations of serum phosphate levels and act to increase or decrease intestinal absorption and renal tubular reabsorption, through the modulation of expression of transcellular transporters at the intestinal and/or renal tubular level. Any acquired or genetic dysfunction in these major organs or regulators may induce hypo- or hyperphosphatemia. The causes of hypo- and hyperphosphatemia are numerous. This review develops the main causes of acquired and genetic hypo- and hyperphosphatemia.

Keywords: Hypophosphatemia; Hyperphosphatemia; Parathyroid hormone; Phosphate depletion; Phosphate regulation; Phosphates; Phosphatonins; Vitamin D

Links

DOI: 10.1007/s00223-020-00664-9

PubMed: 32285168

WoS: 000526248300002

History

Received: 2019-11-04

Accepted: 2020-01-20

Online: 2020-04-13

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Cited By (1)

Year	Entry
2022	Aljuraibah F, Bacchetta J, Brandi ML, Florenzano P, Javaid MK, Mäkitie O, Raimann A, Rodriguez M, Siggelkow H, Tiosano D, Vervloet M, Wagner CA. An expert perspective on phosphate dysregulation with a focus on chronic hypophosphatemia. J Bone Miner Res. January 2022;37(1):12-20.