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TNF Alpha−308 Genotype and Renin-Angiotensin System in Hemodialysis Patients: An Effect on Inflammatory Cytokine Levels?

:  Background: Renin–angiotensin system (RAS) was suggested to modulate inflammatory cytokine production. Angiotensin II was consistently shown to increase production of tumor necrosis factor alpha (TNF‐α). However, inflammatory cytokines and RAS were modulated by genetic polymorphisms such as TNF‐α...

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Published in:Artificial organs 2005-02, Vol.29 (2), p.174-178
Main Authors: Genctoy, Gultekin, Altun, Bulent, Alper Kiykim, Ahmet, Arici, Mustafa, Erdem, Yunus, Çağlar, Meltem, Yasavul, Ünal, Turgan, Çetin, Çağlar, Şali
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Language:English
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Summary::  Background: Renin–angiotensin system (RAS) was suggested to modulate inflammatory cytokine production. Angiotensin II was consistently shown to increase production of tumor necrosis factor alpha (TNF‐α). However, inflammatory cytokines and RAS were modulated by genetic polymorphisms such as TNF‐α−308 G > A and angiotensin‐converting enzyme (ACE) I/D gene polymorphisms. The aim of this study was to investigate the effects of ACE and TNF‐α genotypes on inflammatory cytokines in hemodialysis (HD) patients. Methods: ACE I/D and TNF‐α−308 G > A genotypes, pre‐ and postdialysis plasma renin activity (PRA), serum ACE, interleukin‐1 beta (IL‐1β), and TNF‐α levels were determined in 22 HD patients. Results: Predialysis serum ACE activity is correlated with TNF‐α (r = 0.63; P = 0.01), and PRA was correlated with IL‐1β levels (r = 0.49; P = 0.02). Pre/postdialysis IL‐1β and TNF‐α were similar in DD and II/ID ACE genotypes. Predialysis TNF‐α and IL‐1β (32.4 ± 5; 35.1 ± 4.2 vs. 28.1 ± 3.7; 26.5 ± 6.2 pg/mL; P 
ISSN:0160-564X
1525-1594
DOI:10.1111/j.1525-1594.2005.29029.x