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With or without the kidney: the role of FGF23 in CKD
Author(s) -
Masafumi Fukagawa,
Junichiro James Kazama
Publication year - 2005
Publication title -
nephrology dialysis transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gfh827
Subject(s) - medicine , kidney disease , fibroblast growth factor 23 , kidney , intensive care medicine , calcium , parathyroid hormone
The systemic balance of phosphate is maintained mainly by three organs, i.e. the intestine, kidney and bone. Several factors including parathyroid hormone (PTH) and vitamin D play a critical role in this system. Fibroblast growth factor 23 (FGF23) is a recently identified phosphatonin which also is implicated [1,2]. It has been demonstrated in several diseases that excessive activity of FGF23 resulted in hypophosphataemia, low plasma 1,25-dihydroxyvitamin D (1,25D) levels and osteomalacia [3–5]. In animals, the administration of recombinant FGF23 led to the same results [6]. Furthermore, overexpression of FGF23 led to phosphate wasting [7] and rickets, while ablation of this gene led to hyperphosphatemia and high circulating 1,25D levels [8].

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