Desjardins MP, Sidibe A, Fortier C, Mac-Way F, Marquis K, De Serres S, Lariviere R and Agharazii M

Journal of the American Society of Hypertension : JASH. 2018;12:5-13.

DOI: https://doi.org/10.1016/j.jash.2017.09.013

in chronic kidney disease–related aortic stiffness.

Abstract

Cardiovascular disease (CVD) is the leading cause of mortality in patients with chronic kidney disease (CKD). Aortic stiffness, a nontraditional risk factor, is associated with high rate of mortality in CKD. Using a CKD animal model with medial vascular calcification, we previously reported increased mRNA expression of interleukin-6 (IL-6), tumor necrosis factor (TNF), and interleukin-1β (IL-1β) in calcified aorta. The aim of the study was to investigate the association between IL-6, TNF, IL-1β, and aortic stiffness in end-stage renal disease patients. In a cross-sectional study, we enrolled 351 patients on dialysis. Aortic stiffness was assessed by carotid-femoral pulse wave velocity (cf-PWV), while central pulse pressure and augmentation index were assessed using generalized transfer function applied to the radial artery pressure wave form. Plasma IL-6, TNF, and IL-1β were measured by enzyme-linked immunosorbent assay. IL-6 was associated with cf-PWV adjusted for mean blood pressure (MBP) (standardized β = 0.270; P < .001). In a multivariate adjusted model for age, diabetes, hypertension, CVD, and MBP, IL-6 was still associated with cf-PWV (standardized β = 0.096; P = .026). The impact of age, diabetes, and CVD on cf-PWV was partially mediated by IL-6 in a mediation analysis. However, there were no associations between TNF, IL-1β, and aortic stiffness. While IL-6 was associated with augmentation index (standardized β = 0.224; P < .001) and central pulse pressure (standardized β = 0.162; P = .001) when adjusted for MBP and heart rate, this relationship was not significant after adjusting for potential confounders.This study suggests a potential role of IL-6 for CKD-related aortic stiffness.