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Oxidative Medicine and Cellular Longevity
Volume 2013, Article ID 301982, 15 pages
Review Article

Oxidative Stress and Nucleic Acid Oxidation in Patients with Chronic Kidney Disease

1Division of Nephrology, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, No. 325, Section 2, Cheng-Kung Road, Neihu, Taipei 114, Taiwan
2Graduate Institute of Medical Science, National Defense Medical Center, Taipei 114, Taiwan
3Division of Neurology, Department of Medicine, Taoyuan General Hospital, Ministry of Health and Welfare, Taoyuan 330, Taiwan
4Division of Nephrology, Department of Medicine, Taipei Medical University-Shuang Ho Hospital, Ministry of Health and Welfare, New Taipei City 235, Taiwan
5Graduate Institute of Clinical Medical, Taipei Medical University, Taipei 110, Taiwan
6Graduate Institute of Microbiology and Immunology, National Defense Medical Center, Taipei 114, Taiwan

Received 7 May 2013; Revised 16 July 2013; Accepted 22 July 2013

Academic Editor: Mu-Rong Chao

Copyright © 2013 Chih-Chien Sung et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Patients with chronic kidney disease (CKD) have high cardiovascular mortality and morbidity and a high risk for developing malignancy. Excessive oxidative stress is thought to play a major role in elevating these risks by increasing oxidative nucleic acid damage. Oxidative stress results from an imbalance between reactive oxygen/nitrogen species (RONS) production and antioxidant defense mechanisms and can cause vascular and tissue injuries as well as nucleic acid damage in CKD patients. The increased production of RONS, impaired nonenzymatic or enzymatic antioxidant defense mechanisms, and other risk factors including gene polymorphisms, uremic toxins (indoxyl sulfate), deficiency of arylesterase/paraoxonase, hyperhomocysteinemia, dialysis-associated membrane bioincompatibility, and endotoxin in patients with CKD can inhibit normal cell function by damaging cell lipids, arachidonic acid derivatives, carbohydrates, proteins, amino acids, and nucleic acids. Several clinical biomarkers and techniques have been used to detect the antioxidant status and oxidative stress/oxidative nucleic acid damage associated with long-term complications such as inflammation, atherosclerosis, amyloidosis, and malignancy in CKD patients. Antioxidant therapies have been studied to reduce the oxidative stress and nucleic acid oxidation in patients with CKD, including alpha-tocopherol, N-acetylcysteine, ascorbic acid, glutathione, folic acid, bardoxolone methyl, angiotensin-converting enzyme inhibitor, and providing better dialysis strategies. This paper provides an overview of radical production, antioxidant defence, pathogenesis and biomarkers of oxidative stress in patients with CKD, and possible antioxidant therapies.