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Effects of losartan and enalapril on high-sensitivity C-reactive protein and total antioxidant in renal transplant recipients with renin-angiotensin system polymorphisms

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Date
2008
Author
Argani, H
Ghorbanihaghjo, A
Aghaeishahsavari, M
Noroozianavval, M
Rashtchizadeh, N
Veisi, P
Safa, J
Abediazar, S
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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. Patients and 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+: 1.0 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 <= .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). Conclusion. 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.
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http://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/51534
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