Prooxidative-Antioxidative Balance of Cells in Different Types of Renal Replacement Therapy

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Abstract

Background: Patients suffering from chronic kidney disease (CKD) are exposed to increased oxidative stress and disturbances manifesting in the enzymatic and non-enzymatic antioxidative defence system. The object of the research was to assess the differences between conservative treatment, peritoneal dialysis and haemodialysis in moderating cellular antioxidative agents. Methods: The group examined comprised 145 patients. The activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase were obtained using kinetic methods. The spectrophotometric method established the concentrations of reduced glutathione, albumin, uric acid, glucose, total protein and lipids. Results: The type of treatment determined significant changes in antioxidative enzyme activities and concentrations of non-enzymatic antioxidative compounds. Conclusions: Peritoneal dialysis provides better antioxidant protection than other types of therapy in CKD and should be considered as first-choice treatment despite more metabolic disorders.

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Most cited references 32

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Glucose-6-phosphate dehydrogenase deficiency: a historical perspective.

Ernest Beutler (2008)

Glucose-6-phosphate dehydrogenase deficiency serves as a prototype of the many human enzyme deficiencies that are now known. Since its discovery more than 50 years ago, the high prevalence of the defect and the easy accessibility of the cells that manifest it have made it a favorite tool of biochemists, epidemiologists, geneticists, and molecular biologists as well as clinicians. In this brief historical review, we trace the discovery of this defect, its clinical manifestations, detection, population genetics, and molecular biology.

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Oxidative stress and haemodialysis: role of inflammation and duration of dialysis treatment.

M-J Thévenin, G Lambrey, Z Massy … (2001)

Oxidative stress has long been demonstrated in haemodialysis patients. However, the factors influencing their oxidative status have not been characterized extensively in these patients. Therefore, the present study was designed to investigate the influence of a large number of factors known to be associated with oxidative stress. In the present cross-sectional study, we determined the plasma levels of lipid and protein oxidation markers in 31 non-smoking haemodialysis patients and 18 non-smoking healthy subjects, together with various components of the antioxidant system at the plasma and erythrocyte level. No influence of age, diabetes or iron overload on oxidative markers and plasma and erythrocyte antioxidant systems was detected in these haemodialysis patients. The lack of an association between iron overload and oxidative status may be related to the lower level of plasma ascorbate in haemodialysis patients, since ascorbate favours the generation of free iron from ferritin-bound iron. Interestingly, plasma C reactive protein (CRP) levels measured by highly sensitive CRP assay were correlated positively with plasma levels of thiobarbituric acid reactive substances (r=0.38, P<0.04) and negatively with plasma alpha-tocopherol levels (r=-0.46, P<0.01). Moreover, significant inverse correlations were observed between duration of dialysis treatment and plasma levels of alpha-tocopherol (r=-0.49, P<0.02) and ubiquinol (r=-0.40, P<0.05). Our results suggest that inflammatory status and duration of dialysis treatment are the most important factors relating to oxidative stress in haemodialysis patients.

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Nitric oxide, oxidative stress, and progression of chronic renal failure.

Paul Modlinger, Kyle Wilcox, Mehwish Aslam (2004)

Cellular injury or organ dysfunction from oxidative stress occurs when reactive oxygen species (ROS) accumulate in excess of the host defense mechanisms. The deleterious effect of ROS occurs from 2 principal actions. First, ROS can inactivate mitochondrial enzymes, damage DNA, or lead to apoptosis or cellular hypertrophy. Second, nitric oxide (NO), which is a principal endothelial-derived relaxing factor, reacts with superoxide anion (O2-) to yield peroxynitrite (ONOO-), which is a powerful oxidant and nitrosating agent. The inactivation of NO by O2- creates NO deficiency. Oxidative stress can promote the production of vasoconstrictor molecules and primary salt retention by the kidney. Several hypertensive animal models showed increased activity of nicotine adenine dinucleotide phosphate (NADPH) oxidase, which is the chief source of O2- in the vessel wall and kidneys. NO regulates renal blood flow, tubuloglomerular feedback (TGF), and pressure natriuresis. Animal models of NO deficiency develop hypertension, proteinuria, and glomerulosclerosis. Evidence is presented that chronic renal failure (CRF) is a state of NO deficiency secondary to decreased kidney NO production and/or increased bioinactivation of NO by O2-. Patients with CRF show decreased endothelium-dependent vasodilatation to acetylcholine, have increased markers of oxidative stress, and diminished antioxidant activity. Therapy for oxidative stress has focused on antioxidants and agents that modify the renin-angiotensin system. The effects of such treatments are more compelling in animal models than in human studies.

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Author and article information

Journal

Journal ID (publisher-id): BPU

Journal ID (nlm-ta): Blood Purif

Journal ID (doi): 10.1159/issn.0253-5068

Title: Blood Purification

Publisher: S. Karger AG

ISSN (Print): 0253-5068

ISSN (Electronic): 1421-9735

Publication date Subscription-year: 2014

Publication date (Print): March 2014

Publication date (Electronic): 28 January 2014

Volume: 37

Issue: 1

Pages: 4-11

Affiliations

^aDepartment of Nephrology, Transplantology and Internal Medicine and ^bDepartment of Medical Analysis, Pomeranian Medical University, Szczecin, Poland

Author notes

*Dr. Joanna Stępniewska, Department of Nephrology, Transplantology and Internal Medicine, Pomeranian Medical University, Powstancow Wielkopolskich 72, PL-70-111 Szczecin (Poland), E-Mail asia_stepniewska@wp.pl

Article

Publisher ID: 356806 Other ID: Blood Purif 2014;37:4-11

DOI: 10.1159/000356806

PubMed ID: 24481175

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