Fibroblast growth factor 23 predicts carotid atherosclerosis in individuals without kidney disease. The CORDIOPREV study.


Journal

European journal of internal medicine
ISSN: 1879-0828
Titre abrégé: Eur J Intern Med
Pays: Netherlands
ID NLM: 9003220

Informations de publication

Date de publication:
04 2020
Historique:
received: 31 07 2019
revised: 15 12 2019
accepted: 17 12 2019
pubmed: 4 1 2020
medline: 16 2 2021
entrez: 4 1 2020
Statut: ppublish

Résumé

Fibroblast growth factor 23 (FGF23) is a major determinant of mineral metabolism derangements and emerges as a possible risk factor underlying the negative cardiovascular outcome in CKD patients. However, its contribution in non-CKD individuals is less clear. This cross-sectional study investigated the associations between FGF23 and mineral metabolism parameters and with carotid atherosclerosis in a population at high cardiovascular risk with preserved renal function. We employed 939 subjects with coronary heart disease enrolled in the CORDIOPREV study (mean eGFR=93.0 ± 0.7 ml/min/1.73 m Adjusted for anthropometric factors, FGF23 associated positively with creatinine, phosphate, calcium and 25(OH)-vitaminD and negatively with eGFR and calcitriol. In multivariable-adjusted models all of them were independent contributors to FGF23 levels. FGF23 showed a positive relationship with IMT-CC; both the higher third and fourth quartiles associated significantly with IMT-CC (Beta= 0.135 and 0.187, respectively) and after additional adjustment for established cardiovascular risk factors and morbidities FGF23 remained as a significant contributor to IMT-CC. Logistic regression analysis confirmed its predictive ability to differentiate patients at higher atherosclerotic risk defined by an IMT-CC≥0.7 mm (OR for FGF23 quartiles 3 and 4 vs. 1: 1.860; 95%CI 1.209-2.862 and 2.114; 95%CI 1.339-3.337, respectively). Even in the setting of a normally functioning phosphate-FGF23-calcitriol system, FGF23 independently associated with IMT-CC, a surrogate of atherosclerotic vascular dysfunction. This supports the notion of FGF23 as a predictor of cardiovascular risk independent of renal failure.

Sections du résumé

BACKGROUND
Fibroblast growth factor 23 (FGF23) is a major determinant of mineral metabolism derangements and emerges as a possible risk factor underlying the negative cardiovascular outcome in CKD patients. However, its contribution in non-CKD individuals is less clear. This cross-sectional study investigated the associations between FGF23 and mineral metabolism parameters and with carotid atherosclerosis in a population at high cardiovascular risk with preserved renal function.
METHODS
We employed 939 subjects with coronary heart disease enrolled in the CORDIOPREV study (mean eGFR=93.0 ± 0.7 ml/min/1.73 m
RESULTS
Adjusted for anthropometric factors, FGF23 associated positively with creatinine, phosphate, calcium and 25(OH)-vitaminD and negatively with eGFR and calcitriol. In multivariable-adjusted models all of them were independent contributors to FGF23 levels. FGF23 showed a positive relationship with IMT-CC; both the higher third and fourth quartiles associated significantly with IMT-CC (Beta= 0.135 and 0.187, respectively) and after additional adjustment for established cardiovascular risk factors and morbidities FGF23 remained as a significant contributor to IMT-CC. Logistic regression analysis confirmed its predictive ability to differentiate patients at higher atherosclerotic risk defined by an IMT-CC≥0.7 mm (OR for FGF23 quartiles 3 and 4 vs. 1: 1.860; 95%CI 1.209-2.862 and 2.114; 95%CI 1.339-3.337, respectively).
CONCLUSION
Even in the setting of a normally functioning phosphate-FGF23-calcitriol system, FGF23 independently associated with IMT-CC, a surrogate of atherosclerotic vascular dysfunction. This supports the notion of FGF23 as a predictor of cardiovascular risk independent of renal failure.

Identifiants

pubmed: 31899053
pii: S0953-6205(19)30437-6
doi: 10.1016/j.ejim.2019.12.008
pii:
doi:

Substances chimiques

FGF23 protein, human 0
Fibroblast Growth Factors 62031-54-3
Fibroblast Growth Factor-23 7Q7P4S7RRE

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

79-85

Informations de copyright

Copyright © 2019 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest M.R. received consulting fees or paid advisory boards from Kyowa Kirin and lecture fees from AMGEN, VIPHOR, Fresenius and Kiowa Kirin. The other authors declared no competing interests. The results presented in this paper have not been published previously in whole or part, except in abstract format.

Auteurs

Maria E Rodríguez-Ortiz (ME)

Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Reina Sofia University Hospital/University of Cordoba, Spain.

Juan F Alcalá-Díaz (JF)

Lipid and Atherosclerosis Unit, Department of Internal Medicine (IMIBIC), Reina Sofia University Hospital/University of Cordoba, Avda. Menéndez Pidal s/n. C.P., 14004 Cordoba, Spain; CIBER Fisiopatologia Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Spain.

Antonio Canalejo (A)

Department of Integrated Sciences/Centro de investigacion RENSMA, University of Huelva, Spain.

José D Torres-Peña (JD)

Lipid and Atherosclerosis Unit, Department of Internal Medicine (IMIBIC), Reina Sofia University Hospital/University of Cordoba, Avda. Menéndez Pidal s/n. C.P., 14004 Cordoba, Spain; CIBER Fisiopatologia Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Spain.

Francisco Gómez-Delgado (F)

Lipid and Atherosclerosis Unit, Department of Internal Medicine (IMIBIC), Reina Sofia University Hospital/University of Cordoba, Avda. Menéndez Pidal s/n. C.P., 14004 Cordoba, Spain; CIBER Fisiopatologia Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Spain.

Juan R Muñoz-Castañeda (JR)

Unidad de Gestión Clinica Nefrología, Instituto Maimonides de Investigacion Biomédica de Córdoba (IMIBIC), Reina Sofia University Hospital/University of Cordoba, Spain.

Javier Delgado-Lista (J)

Lipid and Atherosclerosis Unit, Department of Internal Medicine (IMIBIC), Reina Sofia University Hospital/University of Cordoba, Avda. Menéndez Pidal s/n. C.P., 14004 Cordoba, Spain; CIBER Fisiopatologia Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Spain.

Mariano Rodríguez (M)

Unidad de Gestión Clinica Nefrología, Instituto Maimonides de Investigacion Biomédica de Córdoba (IMIBIC), Reina Sofia University Hospital/University of Cordoba, Spain.

José López-Miranda (J)

Lipid and Atherosclerosis Unit, Department of Internal Medicine (IMIBIC), Reina Sofia University Hospital/University of Cordoba, Avda. Menéndez Pidal s/n. C.P., 14004 Cordoba, Spain; CIBER Fisiopatologia Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Spain. Electronic address: jlopezmir@uco.es.

Yolanda Almadén (Y)

Unidad de Gestión Clinica Medicina Interna, Instituto de Biomedicina de Córdoba (IMIBIC), Hospital Universitario Reina Sofía de Córdoba/Universidad de Córdoba, Spain; CIBER Fisiopatologia Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Spain. Electronic address: yolandaalmaden@yahoo.es.

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