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The Causes of Hypo- and Hyperphosphatemia in Humans

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Abstract

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.

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Abbreviations

ALP:

Alkaline phosphatase activity

Ca:

Serum calcium

CKD:

Chronic kidney disease

Cr:

Creatininemia

eGFR:

Estimated glomerular filtration rate

1,25(OH)2D:

1,25-Dihydroxyvitamin D

25(OH)D:

25-Hydroxyvitamin D

iFGF23:

Intact FGF23

Ph:

Serum phosphate

PTH:

Parathormone

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Koumakis, E., Cormier, C., Roux, C. et al. The Causes of Hypo- and Hyperphosphatemia in Humans. Calcif Tissue Int 108, 41–73 (2021). https://doi.org/10.1007/s00223-020-00664-9

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