A Kolonko1, J Chudek2, M Szotowska3, P Kuczera3, A Wiecek3. 1. Department of Nephrology, Transplantation, and Internal Medicine, Medical University of Silesia, Katowice, Poland. Electronic address: uryniusz@wp.pl. 2. Department of Pathophysiology, Medical University of Silesia, Katowice, Poland. 3. Department of Nephrology, Transplantation, and Internal Medicine, Medical University of Silesia, Katowice, Poland.
Abstract
BACKGROUND: There is limited evidence regarding the risk factors influencing vascular injury in kidney transplant recipients, except for accelerated vasculopathy and endothelial dysfunction in the pre-transplantation period of end-stage renal failure. Therefore, we performed a cross-sectional study to evaluate the role of traditional and novel or potential nontraditional risk factors in vascular and endothelial dysfunction in a cohort of stable kidney transplant recipients. METHODS: One hundred forty-two kidney transplant recipients at 8.4 ± 1.8 years after transplantation were enrolled into the study. Different markers of vascular injury, such as carotid intima-media thickness (IMT), pulse wave velocity (PWV), and peripheral arterial tonometry (PAT), were assessed. Inflammatory markers, oxidative stress and endothelial function surrogate markers, adhesion molecules, and parathormone and osteoprotegerin levels were measured. RESULTS: Among traditional risk factors, only age, pre-transplantation diabetes, left ventricular hypertrophy (LVH) and cardiovascular disease (CVD) were related to increased IMT and PWV, whereas PAT values were significantly decreased only in diabetics and patients with CVD and were similar in patients with and without LVH. In multivariate regression analysis, IMT was explained by age, previous CVD episodes, and higher high-sensitivity C-reactive protein levels, and PWV by age and pre-transplantation diabetes. The regression analysis failed to find any significant explanatory variables for PAT. CONCLUSIONS: 1. In stable kidney transplant recipients, age, pre-transplantation diabetes, previous cardiovascular episode, and systemic microinflammation were predictors of vascular injury. 2. PAT is poorly associated with traditional CV risk factors and does not correspond with levels of biochemical markers of endothelial dysfunction in those patients.
BACKGROUND: There is limited evidence regarding the risk factors influencing vascular injury in kidney transplant recipients, except for accelerated vasculopathy and endothelial dysfunction in the pre-transplantation period of end-stage renal failure. Therefore, we performed a cross-sectional study to evaluate the role of traditional and novel or potential nontraditional risk factors in vascular and endothelial dysfunction in a cohort of stable kidney transplant recipients. METHODS: One hundred forty-two kidney transplant recipients at 8.4 ± 1.8 years after transplantation were enrolled into the study. Different markers of vascular injury, such as carotid intima-media thickness (IMT), pulse wave velocity (PWV), and peripheral arterial tonometry (PAT), were assessed. Inflammatory markers, oxidative stress and endothelial function surrogate markers, adhesion molecules, and parathormone and osteoprotegerin levels were measured. RESULTS: Among traditional risk factors, only age, pre-transplantation diabetes, left ventricular hypertrophy (LVH) and cardiovascular disease (CVD) were related to increased IMT and PWV, whereas PAT values were significantly decreased only in diabetics and patients with CVD and were similar in patients with and without LVH. In multivariate regression analysis, IMT was explained by age, previous CVD episodes, and higher high-sensitivity C-reactive protein levels, and PWV by age and pre-transplantation diabetes. The regression analysis failed to find any significant explanatory variables for PAT. CONCLUSIONS: 1. In stable kidney transplant recipients, age, pre-transplantation diabetes, previous cardiovascular episode, and systemic microinflammation were predictors of vascular injury. 2. PAT is poorly associated with traditional CV risk factors and does not correspond with levels of biochemical markers of endothelial dysfunction in those patients.
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