## Background: Patients on chronic hemodialysis (hd) are exposed to oxidative stress. an hd session is used in this study as an in vivo model for studying the influence of heparin on oxidative stress caused partially by activated peripheral blood polymorphonuclear leukocytes (pmnls) during a hd ses
Oxidative Stress Modulation Immediately After Hemodialysis
✍ Scribed by Daryoush Hamidi Alamdari; Malektaj Honarmand; Abdolfattah Sarrafnejad; Abdolreza Varasteh; Mohammad Reza Parizadeh; Majid Ghayour-Mobarhan; Daryoush Fahimi; Elena Kostidou; Apostolos I. Hatzitolios; George Koliakos
- Book ID
- 102140124
- Publisher
- Wiley (John Wiley & Sons)
- Year
- 2009
- Tongue
- English
- Weight
- 83 KB
- Volume
- 38
- Category
- Article
- ISSN
- 0090-2934
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✦ Synopsis
Abstract
AIM
The aim of this study was to estimate oxidative stress (OS) before and after dialysis in hemodialysis (HD) patients and correlate this stress with routine biochemical parameters.
METHOD
Sera of patients (n = 21), under regular HD, were collected 5 minutes before and after an HD session. Oxidative stress was estimated using the pro‐oxidant‐antioxidant assay (PAB), along with routine biochemical parameters in the same sera.
RESULTS
A significant increase of OS value was observed in HD patients 5 minutes after dialysis. Before HD, a significant correlation was established between the PAB values and fasting blood sugar, calcium, and C‐reactive protein (CRP); and an inverse correlation between the PAB values and uric acid, serum creatinine, albumin, and albumin/globulin ratio. This correlation was not obvious after HD. PAB value, after dialysis, correlated significantly only with serum iron and inversely with alanine transaminase.
CONCLUSION
This study found that the already‐increased OS in HD patients is further increased immediately after dialysis. However, factors influencing post‐dialysis OS may be different from pre‐dialysis factors.
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## Abstract ## BACKGROUND Oxidative stress resulting from membranes is dependent on the increase in production of toxic‐free oxygen radicals occurring through the mediation of complement and leukocyte activation. Increased oxidative stress causes morbid results such as erythropoietin resistance, a