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European Journal of Pediatrics
Published in: European Journal of Pediatrics 5/2011

01-05-2011 | Review

Clinical practice

Fibroblast growth factor (FGF)23: a new hormone

Author: Uri S. Alon

Published in: European Journal of Pediatrics | Issue 5/2011

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Abstract

Until a decade ago, two main hormones were recognized as directly affecting phosphate homeostasis and, with that, bone metabolism: parathyroid hormone and 1,25(OH)2 vitamin D (calcitriol). It was only a decade ago that the third major player hormone was found, linking gut, bone, and kidney. The physiologic role of fibrinogen growth factor (FGF)23 is to maintain serum phosphate concentration within a narrow range. Secreted from osteocytes, it modulates kidney handling of phosphate reabsorption and calcitriol production. Genetic and acquired abnormalities in FGF23 structure and metabolism cause conditions of either hyper-FGF23—manifested by hypophosphatemia, low serum calcitriol, and rickets/osteomalacia—or hypo-FGF23, expressed by hyperphosphatemia, high serum calcitriol, and extra-skeletal calcifications. In patients with chronic renal failure, FGF23 levels increase as kidney functions deteriorate and are under investigation to learn if the hormone actually participates in the pathophysiology of the deranged bone and mineral metabolism typical for these patients and, if so, whether it might serve as a therapeutic target. This review addresses the physiology and pathophysiology of FGF23 and its clinical applications.
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Metadata
Title
Clinical practice
Fibroblast growth factor (FGF)23: a new hormone
Author
Uri S. Alon
Publication date
01-05-2011
Publisher
Springer-Verlag
Published in
European Journal of Pediatrics / Issue 5/2011
Print ISSN: 0340-6199
Electronic ISSN: 1432-1076
DOI
https://doi.org/10.1007/s00431-010-1382-5

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