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Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Chronic Kidney Disease and Disproportionally Increased Cardiovascular Damage: Does Oxidative Stress Explain the
Anila Duni1, Vassilios Liakopoulos2, Karolos-Pavlos Rapsomanikis1
1Department of Nephrology, Medical School of the University of Ioannina, Ioannina, Greece.
Insights
Chronic kidney disease (CKD) patients face high cardiovascular disease risk due to increased oxidative stress. This review highlights how oxidative stress contributes to cardiovascular damage and reduced lifespan in CKD.
Area of Science:
- Nephrology
- Cardiology
- Oxidative Stress Research
Background:
- Chronic kidney disease (CKD) is linked to a significantly increased risk of cardiovascular disease (CVD) and reduced lifespan.
- CKD exacerbates oxidative stress through elevated reactive oxygen species (ROS) production and diminished antioxidant defenses.
Purpose of the Study:
- To elucidate the mechanisms by which oxidative stress contributes to cardiovascular complications in CKD.
- To review the role of oxidative stress pathways in the development of left ventricular hypertrophy (LVH) and cardiorenal syndrome.
- To highlight the significance of paraoxonase-1 (PON1) activity in CKD-related cardiovascular risk.
Main Methods:
- Review of existing literature on oxidative stress in CKD and its cardiovascular implications.
- Analysis of pathophysiological pathways including the intrarenal angiotensin system, NADPH oxidase, and xanthine oxidase.
- Examination of the role of impaired antioxidant enzymes like PON1.
Main Results:
- Increased ROS production in CKD, partly mediated by the intrarenal angiotensin system, drives cardiovascular damage.
- Oxidative stress promotes lipid peroxidation, protein carbamylation, endothelial dysfunction, and inflammation, accelerating atherosclerosis.
- Reduced serum PON1 activity in CKD patients is associated with a higher burden of cardiovascular disease.
Conclusions:
- Oxidative stress is a key factor in the pathogenesis of cardiovascular disease in CKD patients.
- Targeting oxidative stress pathways may offer a therapeutic strategy for managing cardiovascular complications in CKD.
- Further research is warranted to evaluate the efficacy of antioxidant therapies in CKD.
Abstract:
Chronic kidney disease (CKD) patients are among the groups at the highest risk for cardiovascular disease and significantly shortened remaining lifespan. CKD enhances oxidative stress in the organism with ensuing cardiovascular damage. Oxidative stress in uremia is the consequence of higher reactive oxygen species (ROS) production, whereas attenuated clearance of pro-oxidant substances and impaired antioxidant defenses play a complementary role. The pathophysiological mechanism underlying the increased ROS production in CKD is at least partly mediated by upregulation of the intrarenal angiotensin system. Enhanced oxidative stress in the setting of the uremic milieu promotes enzymatic modification of circulating lipids and lipoproteins, protein carbamylation, endothelial dysfunction via disruption of nitric oxide (NO) pathways, and activation of inflammation, thus accelerating atherosclerosis. Left ventricular hypertrophy (LVH) and heart failure are hallmarks of CKD. NADPH oxidase activation, xanthine oxidase, mitochondrial dysfunction, and NO-ROS are the main oxidative pathways leading to LVH and the cardiorenal syndrome. Finally, a subset of antioxidant enzymes, the paraoxonases (PON), deserves special attention due to abundant clinical evidence accumulated regarding reduced serum PON1 activity in CKD as a contributor to the increased burden of cardiovascular disease. Future, meticulously designed studies are needed to assess the effects of antioxidant therapy on patients with CKD.
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