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      G-Protein Beta-3-Subunit and eNOS Gene Polymorphism in Transplant Recipients with Long-Term Renal Graft Function

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          Abstract

          Background: Despite new immunosuppressive drugs, only a minority of graft survive over 15 years. The aim of our study was to determine the influence of gene polymorphisms in the G-protein-β<sub>3</sub> subunit (Gβ3) and endothelial nitric oxide synthase (eNOS) on the long-term outcome of kidney grafts. Methods: Using PCR, corresponding genotypes in Gβ3 (C825T) and eNOS (G894T) gene polymorphism were evaluated in patients with preserved graft function over 15 years and in a control group of transplant recipients. Results: There were no differences in allele and genotype distributions of both polymorphisms between groups. In Gβ3 polymorphism, the 825T allele carriers had a significantly lower body mass index while in eNOS polymorphism there were no links between genotypes, renal function and atherosclerosis risk factors. Conclusions: Our data suggest that these gene polymorphisms have only a minor influence on long-term renal graft function.

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          Most cited references 6

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          Association of the Glu298Asp polymorphism in the endothelial nitric oxide synthase gene with essential hypertension resistant to conventional therapy.

          Endothelial nitric oxide synthase (eNOS) produces nitric oxide (NO) which, after diffusing into vascular smooth muscle cells, activates guanylate cyclase leading to vasodilatation. A polymorphism (894G to T) in exon 7 of the eNOS gene causes the conversion of Glu to Asp in position 298. The recently described crystal structure of the heme domain of eNOS protein shows that Glu298 is fully solvent accessible and distant from regions integral to enzyme function. Searching for phenotypic expression of eNOS gene variants, we genotyped a group of patients with essential hypertension (H, n = 119) for the Glu298Asp polymorphism and compared them with age- and sex-matched healthy normals (N, n = 85). To specify phenotypic expression further, the hypertensive patients were subdivided into one group that responded well to regular antihypertensive therapy (CH, n = 45) and one group that was resistant to the therapy (RH, n = 74). Patients with BP higher than 140/90 mmHg when on adequate lifestyle modification and triple-combination therapy (including diuretics) were considered resistant. In RH and H groups, a significantly higher frequency of T alleles (P = 0.022 and P = 0.046, respectively) was found compared to normotonics (N). In well-controlled hypertonics, the same tendency was found, but did not reach statistical significance. The Glu298Asp polymorphism may contribute to the complex pathogenesis of essential hypertension and may be a factor in the resistance of these patients to conventional antihypertensive therapy. The presence of this allele may thus be predictive of the patients' therapeutic response. Copyright 2001 Academic Press.
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            Angiotensin converting enzyme gene I/D polymorphism in essential hypertension and nephroangiosclerosis.

            An insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene significantly influences circulating ACE levels and plays a role in the development of target organ damage, that is, left ventricular hypertrophy in essential hypertension (EH), and microalbuminuria in diabetes mellitus. We have examined the role of the I/D polymorphism in essential hypertensive patients with renal involvement. The study was divided in two independent protocols. In protocol 1, we retrospectively analyzed the ACE genotypes in 37 essential hypertensive patients with a clinical and histopathological diagnosis of nephroangiosclerosis. In protocol 2, ACE genotypes as well as microalbuminuria and renal hemodynamic parameters were investigated in 75 patients with EH with normal renal function and a strong family history of hypertension. As control group, 75 healthy subjects with BP < 130/85 mm Hg and no family history of cardiovascular diseases were studied. The ACE variants were determined by PCR and the genotypes were classified as DD, DI and II. In protocol 1, patients with nephroangiosclerosis displayed a significant difference in the genotype distribution (57% DD, 27% DI, 16% II) when compared to the control population (25% DD, 64% DI, 11% II; P < 0.001). There was no significant difference in genotype distribution between hypertensive patients with normal renal function (protocol 2; 33% DD, 59% DI, 8% II) and the control group. There were no differences in age, blood pressure, microalbuminuria and duration of the disease among the three genotypes in the EH group from protocol 2. Taken together, these findings suggest that the DD genotype of ACE is associated with histopathologic-proven kidney involvement in patients with EH and that this polymorphism could be a potential genetic marker in hypertensives at risk of renal complications.
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              THE EFFECT OF BODY MASS INDEX ON LONG-TERM RENAL ALLOGRAFT SURVIVAL

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                Author and article information

                Journal
                KBR
                Kidney Blood Press Res
                10.1159/issn.1420-4096
                Kidney and Blood Pressure Research
                S. Karger AG
                1420-4096
                1423-0143
                2002
                2002
                08 November 2002
                : 25
                : 4
                : 245-249
                Affiliations
                aDepartment of Nephrology, bLaboratory of Atherosclerosis Research, and cTransplant Center, Institute for Clinical and Experimental Medicine, Prague, Czech Republic; dDepartment of Nephrology, University Clinic, Essen, Germany; eDepartment of Pediatrics, Semmelweis University, Budapest, Hungary
                Article
                66346 Kidney Blood Press Res 2002;25:245–249
                10.1159/000066346
                12424427
                © 2002 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Tables: 3, References: 26, Pages: 5
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/66346
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                Original Paper

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