title: Effects of losartan and enalapril on high-sensitivity C-reactive protein and total antioxidant in renal transplant recipients with Renin-Angiotensin system polymorphisms.
abstract: BACKGROUND
  As renin-angiotensin system (RAS) activity may affect the severity of oxidative stress and inflammatory markers, we assessed the effects of enalapril (E) and/or losartan (L) on these markers in renal transplant recipients with RAS polymorphisms.
  
  
  METHODS
  After determination by PCR of RAS genotypes, consisting of the angiotensin-converting enzymes (ACE I/D), angiotensinogens (AGT M235T) and angiotensin II type 1 receptors (ATR1 A1166C), 76 recipients were recruited randomly and assigned 4 groups. The first (n = 17) and second (n = 24) groups were treated with E (E(+): 10 mg/d) and L (L(+): 50 mg/d) alone, respectively. The third positive control group (n = 17) received E + L (E(+)L(+): 10 mg/d + 50 mg/d) and the fourth negative control group (n = 18) received no medication (E(-):L(-)). High-sensitivity C-reactive protein (hs-CRP) and total antioxidant (TA) inflammatory and antioxidative markers were measured after 2 months. After a 2-week washout period, the E(+) group was changed to L(+) and vice versa in a crossover design. They were followed for another 8 weeks before retesting hs-CRP and TA. A value of P < or = .05 was considered significant.
  
  
  RESULTS
  After 2 and 4 months of treatment with the drug regimen, hs-CRP and TA levels were significantly decreased and consequently increased among the E(+)L(+), L(+) and E(+) groups (P < .05). On analyzing the relationship between RAS polymorphisms and baseline hs-CRP or TA levels, CC genotype of ATR1 showed lower hs-CRP levels (P = .04). However, none of the RAS polymorphisms predicted the antioxidant and anti-inflammatory response rates to the drugs (P > .05).
  
  
  CONCLUSIONS
  Although hs-CRP was lower in the CC genotype patients of ATR1 polymorphisms E and/or L reduced hs-CRP and increased TA regardless of the RAS genotype.
authors.affiliation: Nephrology Department, Shaheed Beheshti Medical University, Tabriz, Iran.
authors.forename: H
authors.initials: H
authors.lastname: Argani
authors.forename: A
authors.initials: A
authors.lastname: Ghorbanihaghjo
authors.forename: M
authors.initials: M
authors.lastname: Aghaeishahsavari
authors.forename: M
authors.initials: M
authors.lastname: Noroozianavval
authors.forename: N
authors.initials: N
authors.lastname: Rashtchizadeh
authors.forename: P
authors.initials: P
authors.lastname: Veisi
authors.forename: J
authors.initials: J
authors.lastname: Safa
authors.forename: S
authors.initials: S
authors.lastname: Abediazar
mesh_terms: D000328:Adult; D000959:Antihypertensive Agents / Q000627:therapeutic use; D000975:Antioxidants / Q000627:therapeutic use*; D002097:C-Reactive Protein / Q000187:drug effects / Q000378:metabolism*; D003404:Creatinine / Q000097:blood; D004656:Enalapril / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D016030:Kidney Transplantation / Q000276:immunology*; D019808:Losartan / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000235:genetics*
chemical_list: D000959:Antihypertensive Agents; D000975:Antioxidants; D004656:Enalapril; D002097:C-Reactive Protein; D003404:Creatinine; D019808:Losartan