Novel Faces of Fibroblast Growth Factor 23 (FGF23): Iron Deficiency, Inflammation, Insulin Resistance, Left Ventricular Hypertrophy, Proteinuria and Acute Kidney Injury

Mehmet Kanbay*, Marc Vervloet, Mario Cozzolino, Dimitrie Siriopol, Adrian Covic, David Goldsmith, Yalcin Solak

*Corresponding author for this work

Research output: Contribution to journalReview articleAcademicpeer-review

Abstract

FGF23 is a hormone that appears as the core regulator of phosphate metabolism. Great deal of data has accumulated to demonstrate increased FGF23 secretion from the bone to compensate for even subtle increases in serum phosphorus long before intact PTH. However, recent evidence points to the fact that actions and interactions of FGF23 are not limited solely to phosphate metabolism. FGF23 may be implicated in iron metabolism and erythropoiesis, inflammation, insulin resistance, proteinuria, acute kidney injury and left ventricular hypertrophy. In this review, we will summarize latest experimental and clinical data examining impact of FGF23 on aforementioned pathophysiologic pathways/disorders.

Original languageEnglish
Pages (from-to)217-228
Number of pages12
JournalCalcified Tissue International
Volume100
Issue number3
DOIs
Publication statusPublished - 1 Mar 2017

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