FGF23 and inflammation-a vicious coalition in CKD

Brian Czaya; Christian Faul

doi:10.1016/j.kint.2019.05.018

FGF23 and inflammation-a vicious coalition in CKD

Kidney Int. 2019 Oct;96(4):813-815. doi: 10.1016/j.kint.2019.05.018.

Authors

Brian Czaya¹, Christian Faul²

Affiliations

¹ Division of Nephrology, Department of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama, USA.
² Division of Nephrology, Department of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama, USA. Electronic address: cfaul@uabmc.edu.

PMID: 31543148
DOI: 10.1016/j.kint.2019.05.018

Abstract

High serum concentrations of the phosphaturic hormone, fibroblast growth factor 23 (FGF23), contribute to various tissue injuries. In chronic kidney disease, the sources of FGF23 and the stimuli that control FGF23 production differ from those in the physiologic scenario. Mediators of inflammation are intensively studied as potential factors that contribute to FGF23 elevations and thereby might function as drug targets to lower FGF23 levels. The present study focuses on tumor necrosis factor.

Publication types

Comment

MeSH terms

Fibroblast Growth Factor-23
Fibroblast Growth Factors
Humans
Hypophosphatemia, Familial*
Inflammation
Renal Insufficiency, Chronic*

Substances

FGF23 protein, human
Fibroblast Growth Factors
Fibroblast Growth Factor-23

Grants and funding

F31 DK117550/DK/NIDDK NIH HHS/United States