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Published on: December 15, 2018
Fibroblast growth factor 23 and left ventricular hypertrophy in chronic kidney disease
Orlando M Gutiérrez1, James L Januzzi, Tamara Isakova
1Division of Nephrology and Hypertension, Department of Medicine, University of Miami Miller School of Medicine, Miami, FL 33136, USA. ogutierrez2@med.miami.edu
Insights
Elevated fibroblast growth factor 23 (FGF-23) is linked to left ventricular hypertrophy in chronic kidney disease (CKD) patients. This study suggests FGF-23 may play a role in cardiac changes seen in CKD.
Area of Science:
- Nephrology
- Cardiology
- Endocrinology
Background:
- Fibroblast growth factor 23 (FGF-23) is a key hormone regulating phosphorus.
- Elevated FGF-23 levels are common in chronic kidney disease (CKD) and linked to mortality.
- FGFs are implicated in myocardial hypertrophy and atherosclerosis, risk factors for mortality in CKD.
Purpose of the Study:
- To investigate the association between elevated FGF-23 concentrations and left ventricular hypertrophy (LVH) in CKD patients.
- To explore the relationship between FGF-23 and coronary artery calcification (CAC) in CKD.
Main Methods:
- A cross-sectional study involving 162 CKD patients and 58 controls.
- Echocardiograms and computed tomography scans were used to assess left ventricular mass index (LVMI) and CAC.
- Multivariable-adjusted regression analyses were performed to determine independent associations.
Main Results:
- Increased FGF-23 was independently associated with higher LVMI and increased risk of LVH in CKD patients.
- These associations were stronger in CKD subjects compared to the overall sample.
- While FGF-23 was linked to CAC, this association lost significance after multivariable adjustment.
Conclusions:
- FGF-23 is independently associated with LVMI and LVH in patients with CKD.
- Further research is needed to determine if elevated FGF-23 is a marker or a causal factor in myocardial hypertrophy in CKD.
Background:
Fibroblast growth factor 23 (FGF-23) is a phosphorus-regulating hormone. In chronic kidney disease (CKD), circulating FGF-23 levels are markedly elevated and independently associated with mortality. Left ventricular hypertrophy and coronary artery calcification are potent risk factors for mortality in CKD, and FGFs have been implicated in the pathogenesis of both myocardial hypertrophy and atherosclerosis. We conducted a cross-sectional study to test the hypothesis that elevated FGF-23 concentrations are associated with left ventricular hypertrophy and coronary artery calcification in patients with CKD.
Methods And Results:
In this study, 162 subjects with CKD underwent echocardiograms and computed tomography scans to assess left ventricular mass index and coronary artery calcification; echocardiograms also were obtained in 58 subjects without CKD. In multivariable-adjusted regression analyses in the overall sample, increased log FGF-23 concentrations were independently associated with increased left ventricular mass index (5% increase per 1-SD increase in log FGF-23; P=0.01) and risk of left ventricular hypertrophy (odds ratio per 1-SD increase in log FGF-23, 2.1; 95% confidence interval, 1.03 to 4.2). These associations strengthened in analyses restricted to the CKD subjects (11% increase in left ventricular mass index per 1-SD increase in log FGF-23; P=0.01; odds ratio of left ventricular hypertrophy per 1-SD increase in log FGF-23, 2.3; 95% confidence interval, 1.2 to 4.2). Although the highest tertile of FGF-23 was associated with a 2.4-fold increased risk of coronary artery calcification > or =100 versus <100 U compared with the lowest tertile (95% confidence interval, 1.1 to 5.5), the association was no longer significant after multivariable adjustment.
Conclusions:
FGF-23 is independently associated with left ventricular mass index and left ventricular hypertrophy in patients with CKD. Whether increased FGF-23 is a marker or a potential mechanism of myocardial hypertrophy in CKD requires further study.
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