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Enalapril and losartan affect lipid peroxidation in renal transplant recipients with renin-angiotensin system polymorphisms

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Date
2007
Author
Rashtchizadeh, N
Aghaeishahsavari, M
Argani, H
Noroozianavval, M
Veisi, P
Ghorbanihaghjo, A
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Abstract
Objectives: In this study, the effect of enalapril (E) and/or losartan (L) on lipid peroxidation (LPO) is studied in renal transplant recipients (RTRs) with regard to polymorphisms of renin-angiotensin system (RAS). Design and methods: After determination of genotypes of the angiotensin-converting enzyme (ACE I/D), angiotensinogen (AGT M235T) and angiotensin II type 1 receptor (ATRI A1166C) by PCR, sixty-four RTRs recruited to four groups randomly: first (13 patients) and second (20 patients) groups were treated with enalapril (E+: 10 mg/day) and losartan (L+: 50 mg/day) alone for 2 months, respectively. After 2 weeks as washout period, E group changed to L and vice versa as a cross-over design and they were treated for another 2 months. The third group (13 patients) as positive control received enalapril + losartan (E+L+:10 mg/day+50 mg/day) for 16 weeks, and the forth group (18 patients) as negative control received no medication (E-L-). Malondialdehyde (MDA) as LPO marker was measured before and after treatment. In this study, P < 0.05 was considered significant. Results: After 2 months of treatment, MDA level significantly decreased in all of the groups except the E-L-. MDA level in pre- vs. postintervention for the E+L+, E+, L+ and E-L- groups were as follows: 5.81 +/- 2.13 nmol/mL vs. 1.61 +/- 0.80 nmol/mL (P=0.001), 5.10 +/- 2.05 nmol/ mL vs. 1.68 +/- 1.01 nmol/mL (P=0.003), 5.20 +/- 1.61 nmol/mL vs. 1.22 +/- 0.27 nmol/mL (P=0.000) and 5.27 +/- 2.12 nmol/mL vs. 5.07 +/- 2.03 nmol/ mL (P=0.52), respectively. Also, the same results were found in the end of 16th week. Although patients with DD genotype of ACE had higher MDA (P=0.01) levels, RAS polymorphisms could not predict the antioxidative response rate to the drugs (P > 0.05). Conclusions: E and/or L reduce MDA regardless of the RAS genotypes. (c) 2006 The Canadian Society of Clinical Chemists. All rights reserved.
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http://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/51762
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