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Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Oxidative stress in chronic kidney disease
Kristien Daenen1,2,3, Asmin Andries4, Djalila Mekahli5,6
1Department of Microbiology and Immunology, Laboratory of Nephrology, KU Leuven - University of Leuven, 3000, Leuven, Belgium. Kristien.daenen@gmail.com.
Oxidative stress (OS) damages cells by generating reactive oxygen and nitrogen species. This review explores OS
Area of Science:
- Nephrology
- Biochemistry
- Pathophysiology
Background:
- Oxidative stress (OS) arises from an imbalance between pro-oxidants and antioxidants, leading to harmful reactive oxygen (ROS) and nitrogen (RNS) species.
- While physiological OS aids cell signaling, excessive ROS/RNS cause molecular damage (lipids, proteins, DNA).
- The kidney's high metabolic activity and mitochondrial oxidation make it susceptible to OS-induced damage, accelerating kidney disease.
Purpose of the Study:
- To review the role of OS in chronic kidney disease (CKD) progression.
- To examine the association between OS and CKD complications.
- To discuss potential antioxidant and pharmacological therapies for OS in CKD patients.
Main Methods:
- Literature review of oxidative stress in kidney disease.
- Analysis of OS's impact on CKD progression and complications.
- Exploration of therapeutic targets for OS reduction.
Main Results:
- OS is implicated in kidney disease due to antioxidant depletion and increased ROS production.
- Advanced CKD is linked to heightened OS, contributing to hypertension, atherosclerosis, inflammation, and anemia.
- OS accelerates the progression of kidney disease.
Conclusions:
- Oxidative stress significantly influences CKD progression and associated complications.
- Antioxidants and pharmacological agents targeting OS present potential therapeutic strategies for CKD.
- Reducing OS may benefit both pediatric and adult CKD patients.
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