Fibroblast Growth Factor 23 Genotype and Cardiovascular Disease in Patients Undergoing Hemodialysis.


Journal

American journal of nephrology
ISSN: 1421-9670
Titre abrégé: Am J Nephrol
Pays: Switzerland
ID NLM: 8109361

Informations de publication

Date de publication:
2019
Historique:
received: 12 09 2018
accepted: 04 12 2018
pubmed: 23 1 2019
medline: 3 4 2020
entrez: 23 1 2019
Statut: ppublish

Résumé

Elevated serum concentrations of fibroblast growth factor 23 (FGF23) are associated with cardiovascular mortality in patients with chronic kidney disease and those undergoing dialysis. We tested the hypotheses that polymorphisms in FGF23, its co-receptor alpha-klotho (KL), and/or FGF23 receptors (FGFR) are associated with cardiovascular events and/or mortality. We used 1,494 DNA samples collected at baseline from the Evaluation of Cinacalcet HCl Therapy to Lower Cardiovascular Events Trial, in which patients were randomized to the calcimimetic cinacalcet or placebo for the treatment of secondary hyperparathyroidism. We analyzed European and African Ancestry samples separately and then combined summary statistics to perform a meta-analysis. We evaluated single-nucleotide polymorphisms (SNPs) in FGF23, KL, and FGFR4 as the key exposures of interest in proportional hazards (Cox) regression models using adjudicated endpoints (all-cause and cardiovascular mortality, sudden cardiac death, and heart failure [HF]) as the outcomes of interest. rs11063112 in FGF23 was associated with cardiovascular mortality (risk allele = A, hazard ratio [HR] 1.32, meta-p value = 0.004) and HF (HR 1.40, meta-p value = 0.007). No statistically significant associations were observed between FGF23 rs13312789 and SNPs in FGFR4 or KL genes and the outcomes of interest. rs11063112 was associated with HF and cardiovascular mortality in patients receiving dialysis with moderate to severe secondary hyperparathyroidism.

Sections du résumé

BACKGROUND
Elevated serum concentrations of fibroblast growth factor 23 (FGF23) are associated with cardiovascular mortality in patients with chronic kidney disease and those undergoing dialysis.
OBJECTIVES
We tested the hypotheses that polymorphisms in FGF23, its co-receptor alpha-klotho (KL), and/or FGF23 receptors (FGFR) are associated with cardiovascular events and/or mortality.
METHODS
We used 1,494 DNA samples collected at baseline from the Evaluation of Cinacalcet HCl Therapy to Lower Cardiovascular Events Trial, in which patients were randomized to the calcimimetic cinacalcet or placebo for the treatment of secondary hyperparathyroidism. We analyzed European and African Ancestry samples separately and then combined summary statistics to perform a meta-analysis. We evaluated single-nucleotide polymorphisms (SNPs) in FGF23, KL, and FGFR4 as the key exposures of interest in proportional hazards (Cox) regression models using adjudicated endpoints (all-cause and cardiovascular mortality, sudden cardiac death, and heart failure [HF]) as the outcomes of interest.
RESULTS
rs11063112 in FGF23 was associated with cardiovascular mortality (risk allele = A, hazard ratio [HR] 1.32, meta-p value = 0.004) and HF (HR 1.40, meta-p value = 0.007). No statistically significant associations were observed between FGF23 rs13312789 and SNPs in FGFR4 or KL genes and the outcomes of interest.
CONCLUSIONS
rs11063112 was associated with HF and cardiovascular mortality in patients receiving dialysis with moderate to severe secondary hyperparathyroidism.

Identifiants

pubmed: 30669147
pii: 000496060
doi: 10.1159/000496060
pmc: PMC6473180
mid: NIHMS1005998
doi:

Substances chimiques

Calcimimetic Agents 0
FGF23 protein, human 0
Fibroblast Growth Factors 62031-54-3
Fibroblast Growth Factor-23 7Q7P4S7RRE
FGFR4 protein, human EC 2.7.10.1
Receptor, Fibroblast Growth Factor, Type 4 EC 2.7.10.1
Glucuronidase EC 3.2.1.31
Klotho Proteins EC 3.2.1.31
Cinacalcet UAZ6V7728S

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

125-132

Subventions

Organisme : NIDDK NIH HHS
ID : R01 DK100306
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR002529
Pays : United States

Informations de copyright

© 2019 S. Karger AG, Basel.

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Auteurs

Tae-Hwi Schwantes-An (TH)

Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, Indiana, USA.

Sai Liu (S)

Division of Nephrology, Department of Medicine, Stanford University School of Medicine, Stanford, California, USA.

Margaret Stedman (M)

Division of Nephrology, Department of Medicine, Stanford University School of Medicine, Stanford, California, USA.

Brian S Decker (BS)

Division of Nephrology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA.

Leah Wetherill (L)

Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, Indiana, USA.

Howard J Edenberg (HJ)

Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana, USA.

Matteo Vatta (M)

Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, Indiana, USA.

Tatiana M Foroud (TM)

Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, Indiana, USA.

Glenn M Chertow (GM)

Division of Nephrology, Department of Medicine, Stanford University School of Medicine, Stanford, California, USA.

Sharon M Moe (SM)

Division of Nephrology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA, smoe@iu.edu.
Roudebush Veterans Administration Medical Center, Indianapolis, Indiana, USA, smoe@iu.edu.

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Classifications MeSH