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Updated: Jun 1, 2026

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Peripheral vascular dysfunction in chronic kidney disease
Christopher R Martens1, David G Edwards
1Department of Kinesiology & Applied Physiology, University of Delaware, 541 South College Avenue, Newark, DE 19716, USA.
Insights
Patients with chronic kidney disease (CKD) face higher cardiovascular disease (CVD) mortality due to endothelial dysfunction. Mechanisms like oxidative stress and uremic toxins impair vascular function, potentially becoming irreversible with disease progression.
Area of Science:
- Nephrology
- Cardiology
- Vascular Biology
Background:
- Chronic kidney disease (CKD) is linked to increased cardiovascular disease (CVD) mortality.
- Endothelial dysfunction is a key factor in atherosclerosis and hypertension, contributing to CVD risk in CKD patients.
- Peripheral vascular dysfunction is observed in moderate to severe CKD.
Purpose of the Study:
- To review current literature on mechanisms of peripheral vascular dysfunction in CKD.
- To identify potential therapeutic targets for treating vascular dysfunction in CKD.
Main Methods:
- Literature review of studies on endothelial function in CKD.
- Analysis of proposed mechanisms including oxidative stress, L-arginine deficiency, and ADMA.
- Examination of cell culture data on uremic toxin effects.
Main Results:
- Oxidative stress, L-arginine deficiency, and elevated ADMA contribute to endothelial dysfunction in CKD.
- Uremic toxins may inhibit L-arginine transport and reduce nitric oxide production.
- Endothelial dysfunction may be less reversible as CKD progresses.
Conclusions:
- Understanding the mechanisms of vascular dysfunction is crucial for managing CVD risk in CKD.
- Targeting pathways affected by uremic toxins may offer therapeutic strategies.
- Early intervention may be necessary to prevent irreversible vascular damage.
Abstract:
There is an increased prevalence of cardiovascular disease- (CVD-) related mortality in patients with chronic kidney disease (CKD). Endothelial dysfunction is a primary event in the development of atherosclerosis and hypertension and likely contributes to the elevated cardiovascular risk in CKD. Endothelial dysfunction has been shown to occur in the peripheral vasculature of patients with both severe and moderate CKD. Mechanisms include oxidative stress, L-arginine deficiency, and elevated plasma levels of ADMA. Interventions designed to restore vascular function in patients with CKD have shown mixed results. Evidence from cell culture studies suggest that the accumulation of uremic toxins inhibits L-arginine transport and reduces nitric oxide production. The results of these studies suggest that endothelial dysfunction may become less reversible with advancing kidney disease. The purpose of this paper is to present the current literature pertaining to potential mechanisms of peripheral vascular dysfunction in chronic kidney disease and to identify possible targets for treatment.
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