Changes in the inflammatory and oxidative stress markers during a single hemodialysis session in patients with chronic kidney disease
Background: Cardiovascular disease (CVD) is a common cause of morbidity and mortality in end-stage renal disease (ESRD) patients on hemodialysis (HD) among whom it is 5-20 times higher than in the general population. Some of the nontraditional risk factors such as oxidative stress and inflammation a...
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Published in: | Renal failure Vol. 40; no. 1; pp. 534 - 540 |
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Main Authors: | , , , , |
Format: | Journal Article |
Language: | English |
Published: |
England
Taylor & Francis
01-11-2018
Taylor & Francis Ltd Taylor & Francis Group |
Subjects: | |
Online Access: | Get full text |
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Summary: | Background: Cardiovascular disease (CVD) is a common cause of morbidity and mortality in end-stage renal disease (ESRD) patients on hemodialysis (HD) among whom it is 5-20 times higher than in the general population. Some of the nontraditional risk factors such as oxidative stress and inflammation are related to the progress of CVD in HD patients. Several, but not all studies, reported that inflammatory and oxidative stress markers are increased during a single session of HD, mimicking changes that occur during acute immune activation. This study was taken up to evaluate the changes in the inflammatory and oxidative stress markers during a single HD session in patients with chronic kidney disease.
Methods: Twenty-five ESRD patients on maintenance HD and 25 controls were included in the study. Blood samples were obtained from the patients before starting of hemodialysis (pre-HD) and after completion of hemodialysis (post-HD). The changes in serum Pentraxin-3, hs-CRP, malondialdehyde (MDA) and ferric reducing ability of plasma (FRAP) levels were measured in pre- and post-HD ESRD patients and compared with healthy control group.
Results: This study found increased levels of Pentraxin-3, hs-CRP, MDA, and decreased level of FRAP in HD patients compared to controls.
Conclusions: Hemodialysis procedure contributes to inflammation and oxidative stress. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0886-022X 1525-6049 |
DOI: | 10.1080/0886022X.2018.1487857 |