Fibroblast Growth Factor-23 and Death, Heart Failure, and Cardiovascular Events in Community-Living Individuals CHS (Cardiovascular Health Study)

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY

卷:60

Article

Ix, Joachim H.^1,2,3  Katz, Ronit⁴  Kestenbaum, Bryan R.^5,6  de Boer, Ian H.^5,6  Chonchol, Michel⁷  Mukamal, Kenneth J.⁸  Rifkin, Dena^1,2,3  Siscovick, David S.^9,10  Sarnak, Mark J.¹¹  Shlipak, Michael G.^12,13,14 

[1] Vet Affairs San Diego Healthcare Syst, Nephrol Sect, San Diego, CA USA

[2] Univ Calif San Diego, Div Nephrol, San Diego, CA 92161 USA

[3] Univ Calif San Diego, Div Prevent Med, San Diego, CA 92161 USA

[4] Univ Washington, Collaborat Hlth Studies Coordinating Ctr, Dept Biostat, Seattle, WA 98195 USA

[5] Univ Washington, Div Nephrol, Seattle, WA 98195 USA

[6] Univ Washington, Dept Med, Kidney Res Inst, Seattle, WA 98195 USA

[7] Univ Colorado Denver, Div Renal Dis & Hypertens, Dept Med, Aurora, CO USA

[8] Beth Israel Deaconness Med Ctr, Div Gen Med & Primary Care, Boston, MA USA

[9] Univ Washington, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA

[10] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA

[11] Tufts Med Ctr, Div Nephrol, Dept Med, Boston, MA USA

[12] San Francisco VA Med Ctr, Gen Internal Med Sect, San Francisco, CA USA

[13] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA

[14] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA

关键词: cardiovascular disease;    elderly;    fibroblast growth factor-23;    heart failure;    kidney disease;    mineral metabolism;   

DOI  :  10.1016/j.jacc.2012.03.040

来源: Elsevier

【 摘 要 】

Objectives This study sought to determine the association of fibroblast growth factor (FGF)-23 with death, heart failure (HF), and cardiovascular disease (CVD) in the general population, as well as the influence of chronic kidney disease (CKD) in this setting. Background FGF-23 increases renal phosphorus excretion and inhibits vitamin D activation. In end-stage renal disease, high FGF-23 levels are associated with mortality. The association of FGF-23 with death, HF, and CVD in the general population, and the influence of CKD in this setting, are unknown. Methods Plasma FGF-23 was measured in 3,107 community-living persons >= 65 years of age in 1996 and 1997, and participants were followed through 2008. HF and CVD events were adjudicated by a panel of experts. Associations of FGF-23 with each outcome were evaluated using Cox proportional hazards models, and we tested whether associations differed by CKD status. Results Both lower estimated glomerular filtration rate and higher urine albumin to creatinine ratios were associated with high FGF-23 at baseline. During 10.5 years (median) follow-up, there were 1,730 deaths, 697 incident HF events, and 797 incident CVD events. Although high FGF-23 concentrations were associated with each outcome in combined analyses, the associations were consistently stronger for those with CKD (p interactions all <0.006). In the CKD group (n = 1,128), the highest FGF-23 quartile had adjusted hazards ratios (HR) of 1.87 (95% confidence interval [CI]: 1.47 to 2.38) for all-cause death, 1.94 (95% CI: 1.32 to 2.83) for incident HF, and 1.49 (95% CI: 1.02 to 2.18) for incident CVD events compared with the lowest quartile. Corresponding HRs in those without CKD (n = 1,979) were 1.29 (95% CI: 1.05 to 1.59), 1.37 (95% CI: 0.99 to 1.89), and 1.07 (95% CI: 0.79 to 1.45). Conclusions FGF-23, a hormone involved in phosphorous and vitamin D homeostasis, is independently associated with all-cause death and incident HF in community-living older persons. These associations appear stronger in persons with CKD. (J Am Coll Cardiol 2012;60:200-7) (c) 2012 by the American College of Cardiology Foundation

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