The fibroblast growth factor-23 and Vitamin D emerge as nontraditional risk factors and may affect cardiovascular risk

2014 ◽  
Vol 277 (3) ◽  
pp. 318-330 ◽  
Author(s):  
S. Masson ◽  
N. Agabiti ◽  
T. Vago ◽  
M. Miceli ◽  
F. Mayer ◽  
...  
Keyword(s):  
Risk Factors ◽  
Vitamin D ◽  
Cardiovascular Risk ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth

Abstract P222: Serum fibroblast growth factor-23 and risk of incident stroke: The Atherosclerosis Risk in Communities Study (ARIC)

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Pamela L Lutsey ◽  
Elizabeth Selvin ◽  
Jeffrey R Misialek ◽  
Erin D Michos ◽  
Casey M Rebholz ◽  
...  
Keyword(s):  
Risk Factors ◽  
Vitamin D ◽  
Cardiovascular Risk ◽  
Growth Factor ◽  
Kidney Function ◽  
Stroke Risk ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth ◽  
Increased Risk

Background: Fibroblast growth factor-23 (FGF23), a hormone involved in phosphorous regulation and vitamin D metabolism, has been associated with risk of coronary heart disease and heart failure and is a potential target for intervention. FGF23 may influence stroke risk through several pathways: suboptimal vitamin D levels, impaired kidney function, endothelial dysfunction, and/or inflammation. We tested whether elevated FGF23 is associated with increased risk of incident stroke, independent of traditional stroke risk factors and kidney function. Methods: Biologically active intact FGF23 was measured in stored samples collected at baseline, in 1990-1992, from 12,432 stroke-free ARIC participants. Participants were followed through 2010. Incident stroke events (both ischemic and hemorrhagic) were identified during follow-up and adjudicated using medical chart review. Multivariable Cox proportional hazards regression models were used to evaluate the independent association of baseline serum FGF23 with risk of incident stroke. Results: Over a median follow-up of 19 years, 766 participants (median age 56, 24% black) developed incident stroke. A significant association of baseline FGF23 with incident stroke was only observed in the highest quintile of serum FGF23. Compared to those in the lowest quintile of FGF23, those in the highest quintile were at 37% greater risk of incident stroke (Table), after adjustment for demographics, behaviors, and body mass index. Additional adjustment for cardiovascular risk factors and eGFR categories completely attenuated the association. There was no evidence of interaction by age, sex, race, or eGFR category. Conclusions: Elevated levels of serum FGF23 were associated with modestly increased risk of incident stroke in this large, biracial, community-based cohort in minimally-adjusted models, however this association was not independent of cardiovascular risk factors and kidney function.

scholarly journals Increased Levels of sRAGE in Diabetic CKD-G5D Patients: A Potential Protective Mechanism against AGE-Related Upregulation of Fibroblast Growth Factor 23 and Inflammation

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Elena Dozio ◽  
Valentina Corradi ◽  
Elena Vianello ◽  
Elisa Scalzotto ◽  
Massimo de Cal ◽  
...  
Keyword(s):  
Cardiovascular Risk ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Cardiac Remodeling ◽  
Glycated Albumin ◽  
Fibroblast Growth Factor 23 ◽  
Protective Mechanism ◽  
Fibroblast Growth ◽  
Increased Risk ◽  
Fgf 23

Advanced glycation end products (AGEs) may induce cardiac remodeling in kidney disease by promoting fibroblast growth factor 23 (FGF-23) expression. Since AGEs are increased in diabetes mellitus (DM), our first aim was to evaluate the existence of any potential association between AGEs, FGF-23, inflammation, and increased cardiovascular risk in DM patients on dialysis (CKD-G5D). Secondarily, we explored the potential role of the soluble receptor for AGEs (sRAGE) as a marker of heart failure. Levels of glycated albumin (GA), sRAGE, c-terminal FGF-23 (cFGF-23), brain natriuretic peptide (BNP), and inflammatory mediators were compared between DM and non-DM CKD-G5D patients. The levels of sRAGE, cFGF-23, BNP, and proinflammatory markers were over the ranges of normality in both DM and non-DM groups. Only GA and sRAGE levels were increased in DM compared to non-DM patients. Plasma levels of sRAGE and CRP were the only independent predictors of BNP concentration. In conclusion, in DM CKD-G5D patients, sRAGE appeared to be a marker of cardiac remodeling. Indeed, its increase could be a potential protective mechanism against the increased risk of cardiovascular complications related to AGEs and inflammation. The causal relationship between sRAGE and cardiovascular risk in these patients needs to be further confirmed by mechanistic studies.

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