• Calcif. Tissue Int. · Mar 2017

    Review

    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, and Yalcin Solak.
    • Division of Nephrology, Department of Medicine, Koc University School of Medicine, Sariyer, Istanbul, Turkey. mkanbay@ku.edu.tr.
    • Calcif. Tissue Int. 2017 Mar 1; 100 (3): 217-228.

    AbstractFGF23 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.

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