[FGF23 and the Heart]

Overview

Journal G Ital Nefrol

Specialty Nephrology

Date 2014 Dec 16

PMID 25504170

Citations 5

Authors

I Ezumba

L D Quarles

C P Kovesdy

Affiliations

Soon will be listed here.

Abstract

The prevalence of chronic kidney disease (CKD) has now reached epidemic proportions and it is very likely that it will continue to rise with the increasing prevalence of juvenile diabetes mellitus, hypertension and aging population. CKD is a risk factor for cardiovascular disease (CVD) and cardiovascular disease can lead to CKD. It is also well known that patients with CKD have a higher risk of death from CVD than of progressing to end-stage renal disease that requires renal replacement therapy. In patients with CKD, there is a higher mortality from sudden cardiac death and congestive heart failure than coronary artery disease, which is not the case in the general population. The high prevalence of congestive heart failure in CKD is due to cardiac remodeling which progresses from concentric remodeling to concentric and eccentric hypertrophy, leading to left ventricular hypertrophy with both systolic and diastolic dysfunction. Recent studies have suggested that, in patients with chronic kidney disease, common traditional risk factors for cardiovascular disease such as hypertension, hyperlipidemia and obesity may not be the main determinants of cardiovascular disease. Among the various non-traditional cardiovascular risk factors present in patients with chronic kidney disease, abnormalities of CKD related mineral and bone disorder, which includes elevated fibroblast growth factor 23 (FGF23) have been one of the most extensively studied. However, after many years of research, the debate over the exact pathways by which FGF23 may lead to increased CVD still continues. FGF23 may have both direct and indirect effects on the cardiovascular system. Better understanding of the most relevant pathophysiologic pathways for FGF23 may lead to therapeutic interventions against cardiovascular disease in patients with CKD.

Citing Articles

Fibroblast growth factor-23 and the risk of cardiovascular diseases and mortality in the general population: A systematic review and dose-response meta-analysis.

Liu M, Xia P, Tan Z, Song T, Mei K, Wang J Front Cardiovasc Med. 2022; 9:989574.

PMID: 36407457 PMC: 9669381. DOI: 10.3389/fcvm.2022.989574.

Fam20C in Human Diseases: Emerging Biological Functions and Therapeutic Implications.

Xu R, Tan H, Zhang J, Yuan Z, Xie Q, Zhang L Front Mol Biosci. 2022; 8:790172.

PMID: 34988120 PMC: 8721277. DOI: 10.3389/fmolb.2021.790172.

Serum NGAL and FGF23 may have certain value in early diagnosis of CIN.

Li H, Yu Z, Gan L, Peng L, Zhou Q Ren Fail. 2018; 40(1):547-553.

PMID: 30278796 PMC: 6171456. DOI: 10.1080/0886022X.2018.1487860.

FGF23 promotes myocardial fibrosis in mice through activation of β-catenin.

Hao H, Li X, Li Q, Lin H, Chen Z, Xie J Oncotarget. 2016; 7(40):64649-64664.

PMID: 27579618 PMC: 5323105. DOI: 10.18632/oncotarget.11623.

Phosphate binders for the treatment of chronic kidney disease: role of iron oxyhydroxide.

Cernaro V, Santoro D, Lacquaniti A, Costantino G, Visconti L, Buemi A Int J Nephrol Renovasc Dis. 2016; 9:11-9.

PMID: 26893577 PMC: 4749089. DOI: 10.2147/IJNRD.S78040.

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