Skip Navigation



NDT Advance Access published online on May 9, 2009
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfp205
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
24/10/3125    most recent
gfp205v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Mirza, M. A. I.
Right arrow Articles by Larsson, T. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mirza, M. A. I.
Right arrow Articles by Larsson, T. E.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 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


Relationship between circulating FGF23 and total body atherosclerosis in the community

Majd A. I. Mirza1, Tomas Hansen2, Lars Johansson2, Håkan Ahlström2, Anders Larsson1, Lars Lind1 and Tobias E. Larsson1,3

1 Department of Medical Sciences 2 Department of Oncology, Radiology and Clinical Immunology, Uppsala University Hospital, Uppsala, Sweden 3 Department of Nephrology, Karolinska University Hospital, Stockholm, Sweden

Correspondence and offprint requests to: Tobias E. Larsson; E-mail: tobias.larsson{at}medsci.uu.se



  Abstract

Background. Fibroblast growth factor-23 (FGF23) is a regulator of mineral metabolism and has been suggested to play a role in vascular calcification in chronic kidney disease (CKD). Data on the association between FGF23 and atherosclerosis, both in CKD and in the community, is limited.

Methods. The total body atherosclerosis score (AS) was determined by a magnetic resonance imaging-based angiography in 306 elderly men and women, representing a subsample of the community-based PIVUS cohort. Subjects were divided into three categories based on AS: AS = 0, low AS and high AS. Serum FGF23 was measured using a two-site monoclonal antibody ELISA.

Results. In continuous and multi-category regression models, higher FGF23 was associated with a significant increase in the odds of having a high AS (OR 1.43, CI 1.06–1.92 to OR 3.01, CI 1.52–5.99). This association was stronger in individuals with eGFR <60 mL/min/1.73 m2 (n = 27), reaching a nearly 6-fold increase in the odds for a high AS in the upper FGF23 tertile (OR 5.64, CI 2.78–11.5). We found weaker support for a relationship between FGF23 and the presence of atherosclerosis as subjects in the highest FGF23 tertile had an increased risk for an AS > 0 in crude models (OR 1.93, CI 1.05–3.55), but this was not statistically significant in adjusted (OR 1.42, CI 0.74–1.72) models.

Conclusions. We provide novel evidence supporting an association between serum FGF23 and total body atherosclerosis in the community. Additional studies are warranted to determine the prospective relationship between FGF23 and atherosclerosis, and whether FGF23 is a modifiable cardiovascular risk factor.

Keywords: atherosclerosis; calcification; chronic kidney disease; FGF23; phosphate

Received for publication: 21. 1.09
Accepted in revised form: 15. 4.09


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.