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Published on: July 19, 2018
Fibroblast growth factor 23 is associated with left ventricular hypertrophy, not with uremic vasculopathy in
Insights
Fibroblast growth factor 23 (FGF23) is linked to left ventricular hypertrophy (LVH) in peritoneal dialysis (PD) patients. This study found FGF23 is associated with LVH but not endothelial dysfunction, arterial stiffness, or vascular calcification in PD patients.
Area of Science:
- Nephrology
- Cardiology
- Endocrinology
Background:
- Cardiovascular events are a major cause of death in chronic kidney disease (CKD) patients, including those on peritoneal dialysis (PD).
- Fibroblast growth factor 23 (FGF23) is implicated in left ventricular hypertrophy (LVH) and mortality in CKD patients.
- The specific role of FGF23 in uremic vasculopathy is not fully understood.
Purpose of the Study:
- To investigate the relationship between FGF23 and LVH, endothelial dysfunction, vascular calcification, and arterial stiffness in stable PD patients.
Main Methods:
- Assessed left ventricular mass index (LVMI) via 2-D echocardiography.
- Measured intact FGF23 blood levels using ELISA.
- Evaluated endothelial dysfunction (reactive hyperemia index, RHI) and arterial stiffness (augmentation index, AI) using peripheral arterial tonometry.
- Assessed vascular calcification (VC) using the Adragão score.
Main Results:
- FGF23 positively correlated with serum phosphate, urea, creatinine, dialysis vintage, and LVMI.
- FGF23 negatively correlated with age and residual renal function.
- Multivariate analysis confirmed FGF23 is associated with LVMI, serum phosphate, and age, independent of other factors.
- No significant associations were found between FGF23 and RHI, AI, or VC.
Conclusions:
- FGF23 is associated with LVH in PD patients.
- FGF23 is not associated with endothelial dysfunction, arterial stiffness, or vascular calcification in this population.
Aims:
Cardiovascular (CV) events are the leading cause of morbidity and mortality in patients with chronic kidney disease (CKD), including those patients on peritoneal dialysis (PD). Fibroblast growth factor 23 (FGF23) has been associated with left ventricular hypertrophy (LVH) and mortality in patients with CKD. However, the role of FGF23 in uremic vasculopathy remains unclear. In this study, we aimed to assess the relationship between FGF23 and LVH, endothelial dysfunction, vascular calcification, and arterial stiffness in 48 stable PD patients.
Methods:
Left ventricular mass index (LVMI) was assessed using 2-D echocardiography. Intact FGF23 blood levels were evaluated using an ELISA kit (Immutopics, Inc., San Clemente, CA, USA). Reactive hyperemia index (RHI) is a surrogate marker of endothelial dysfunction and the augmentation index (AI) is a surrogate marker of arterial stiffness. Both were assessed using peripheral arterial tonometry (EndoPAT 2000). Vascular calcification (VC) was assessed using the Adragão score.
Results:
In unadjusted analysis; FGF23 was positively correlated with serum Pi (r = 0.487, p < 0.001), serum urea (r = 0.351, p = 0.015), serum creatinine (r = 0.535, p < 0.001), dialysis vintage (r = 0.309, p = 0.033), and LVMI (r = 0.369, p = 0.027) and was negatively correlated with age (r = -0.343, p = 0.017), residual renal function (r = -0.359, p < 0.012), and AI (r = -0.304, p = 0.038). In multivariate adjusted analysis, FGF23 was associated with LVMI (β = 0.298, p = 0.041), serum Pi (β = 0.345, p = 0.018), and age (β = -0.372, p = 0.007) independent of dialysis vintage, gender, residual renal function (RRF), albumin, C-reactive protein and systolic blood pressure. There were no associations found between FGF23 and RHI, AI, or VC in multivariable- adjusted models.
Conclusions:
Our results show that FGF23 is associated with LVH but not with endothelial dysfunction, arterial stiffness, or vascular calcification in PD patients.
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