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NDT Advance Access originally published online on January 15, 2009
Nephrology Dialysis Transplantation 2009 24(4):1078-1081; doi:10.1093/ndt/gfn688
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© The Author [2009]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


FGF-23 in dialysis patients: ready for prime time?*

Carmine Zoccali

Nephrology, Dialysis and Transplantation Unit and CNR-IBIM Clinical Epidemiology and Pathophysiology of Renal Diseases and Hypertension, Reggio Calabria, Italy

Correspondence and offprint requests to: Carmine Zoccali CNR-IBIM, presso Euroline, Via Vallone Petrara 57, 89124 Reggio Calabria, Italy. Tel: +0039-0965-397010; Fax: +0039-0965-397000; E-mail: carmine.zoccali@tin.it

Keywords: CKD; dialysis; ESRD; FGF-23; survival

The first 150 words of the full text of this article appear below.



   Summary
 
The discovery that fibroblast growth factor 23 (FGF-23) intimately connects skeletal biology and systemic mineral balance is one of the major breakthroughs of the last decade in renal medicine. In a recent observational study by Gutiérrez et al. [2] high FGF-23 levels emerged as a much strong predictor of death and the predictive power of this peptide was maintained even when this relationship was analysed within serum phosphate levels quartiles. Because FGF-23 levels can be lowered by reducing phosphate intake, provided that the FGF-23-death link is causal, the perspective arises that patients with normal phosphate levels but high FGF-23 may be targeted to a phosphate level lower than that currently recommended by guidelines.

Replicating these novel findings in different populations and in diverse clinical settings would give strength to the hypothesis that high FGF-23 is causally involved in the high mortality of dialysis patients. Yet these studies . . . [Full Text of this Article]

Background
The bench to beside paradigm and FGF-23
Causality in epidemiologic studies and FGF-23
Where we go from here

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