title: TNF alpha-308 genotype and renin-angiotensin system in hemodialysis patients: an effect on inflammatory cytokine levels?
abstract: 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-alpha). However, inflammatory cytokines and RAS were modulated by genetic polymorphisms such as TNF-alpha-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-alpha genotypes on inflammatory cytokines in hemodialysis (HD) patients.
  
  
  METHODS
  ACE I/D and TNF-alpha-308 G > A genotypes, pre- and postdialysis plasma renin activity (PRA), serum ACE, interleukin-1 beta (IL-1beta), and TNF-alpha levels were determined in 22 HD patients.
  
  
  RESULTS
  Predialysis serum ACE activity is correlated with TNF-alpha (r = 0.63; P = 0.01), and PRA was correlated with IL-1beta levels (r = 0.49; P = 0.02). Pre/postdialysis IL-1beta and TNF-alpha were similar in DD and II/ID ACE genotypes. Predialysis TNF-alpha and IL-1beta (32.4 +/- 5; 35.1 +/- 4.2 vs. 28.1 +/- 3.7; 26.5 +/- 6.2 pg/mL; P < 0.05) and postdialysis TNF-alpha levels (30.4 +/- 1.4 vs. 28.4 +/- 0.82 pg/mL; P < 0.05) were significantly higher in TNF1/2 than TNF1/1 patients.
  
  
  CONCLUSIONS
  ACE and TNF-alpha-308 G > A (1/2) gene polymorphisms may contribute to modulation of proinflammatory cytokine production and hence chronic inflammation in HD patients.
authors.affiliation: Department of Internal Medicine, Division of Nephrology Hacettepe University Faculty of Medicine, Ankara, Turkey.
authors.forename: Gultekin
authors.initials: G
authors.lastname: Genctoy
authors.forename: Bulent
authors.initials: B
authors.lastname: Altun
authors.forename: Ahmet Alper
authors.initials: AA
authors.lastname: Kiykim
authors.forename: Mustafa
authors.initials: M
authors.lastname: Arici
authors.forename: Yunus
authors.initials: Y
authors.lastname: Erdem
authors.forename: Meltem
authors.initials: M
authors.lastname: Cağlarg
authors.forename: Unal
authors.initials: U
authors.lastname: Yasavul
authors.forename: Cetin
authors.initials: C
authors.lastname: Turgan
authors.forename: Sali
authors.initials: S
authors.lastname: Cağlar
mesh_terms: D000328:Adult; D016207:Cytokines / Q000096:biosynthesis* / Q000097:blood; D005260:Female; D005838:Genotype; D006801:Humans; D007676:Kidney Failure, Chronic / Q000276:immunology* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics / Q000276:immunology; D011110:Polymorphism, Genetic; D006435:Renal Dialysis; D012084:Renin-Angiotensin System / Q000235:genetics / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics* / Q000276:immunology
chemical_list: D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha; D007703:Peptidyl-Dipeptidase A