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Vol. 36, No. 1, 2013
Issue release date: June 2013
Section title: Paper
Blood Purif 2013;36:52-57
(DOI:10.1159/000351001)

FGF23: A Mature Renal and Cardiovascular Risk Factor?

Zoccali C. · Yilmaz M.I. · Mallamaci F.
aNephrology, Hypertension and Renal Transplantation Division and CNR-IBIM Clinical Epidemiology of Renal Diseases and Hypertension, Ospedali Riuniti, Reggio Calabria, Italy; bDepartment of Nephrology, Gulhane School of Medicine, Etlik-Ankara, Turkey

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Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: 5/25/2013

Number of Print Pages: 6
Number of Figures: 2
Number of Tables: 0

ISSN: 0253-5068 (Print)
eISSN: 1421-9735 (Online)

For additional information: http://www.karger.com/BPU

Abstract

High FGF23 predicts renal function loss in chronic kidney disease (CKD) patients and graft failure in transplant patients. FGF23, parathyroid hormone and serum phosphate are all interrelated but among these CKD-MBD biomarkers only FGF23 is independently related with CKD progression. High FGF23 associates with endothelial dysfunction in CKD patients and in elderly individuals in the general population. Furthermore, independently of serum phosphate, high FGF23 associates with mortality and left ventricular hypertrophy in dialysis patients and with atherosclerosis in elderly individuals in the general population. FGF23 also predicts a high risk for death and cardiovascular events in predialysis CKD patients and in subjects with coronary artery disease. A recent trial in CKD patients showed that low phosphate intake associated with a phosphate binder produces a 35% decrease in plasma FGF23. Yet in this and in another trial testing several phosphate binders, FGF23 levels remained well beyond the upper limit of the normal range. Of note, in this latter study, calcification of the coronary arteries and abdominal aorta actually increased, rather than decreased, during treatment with these drugs in the face of evidence of negative phosphate balance and amelioration of hyperparathyroidism. Mechanistic studies are still needed before testing the hypothesis that FGF23 is implicated in a causal manner in cardiovascular and renal diseases. Given the modest effects of phosphate binders on serum FGF23 in CKD patients, pharmacologic interventions antagonizing the effects of this growth factor rather than phosphate-lowering interventions should be put in place to properly test this hypothesis in the clinical scenario in CKD.


  

Author Contacts

Carmine Zoccali
Unità Operativa di Nefrologia e CNR-IBIM
Ospedali Riuniti
IT-89124 Reggio Calabria (Italy)
E-Mail carmine.zoccali@tin.it

  

Article Information

Published online: May 25, 2013
Number of Print Pages : 6
Number of Figures : 2, Number of Tables : 0, Number of References : 52

  

Publication Details

Blood Purification

Vol. 36, No. 1, Year 2013 (Cover Date: June 2013)

Journal Editor: Ronco C. (Vicenza)
ISSN: 0253-5068 (Print), eISSN: 1421-9735 (Online)

For additional information: http://www.karger.com/BPU


Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: 5/25/2013

Number of Print Pages: 6
Number of Figures: 2
Number of Tables: 0

ISSN: 0253-5068 (Print)
eISSN: 1421-9735 (Online)

For additional information: http://www.karger.com/BPU


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