No Effect of Angiotensin-Converting Enzyme Gene Polymorphism on Disease Progression and Left Ventricular Hypertrophy in Autosomal Dominant Polycystic Kidney Disease
Background: Autosomal dominant polycystic kidney disease (ADPKD) shows a variable clinical course suggesting that genetic modifiers might play a role. There are conflicting results about the effect of angiotensin-converting enzyme (ACE) gene polymorphism on the progression of renal failure in ADPKD....
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| Veröffentlicht in: | American journal of nephrology 2003-11, Vol.23 (6), p.466-470 |
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| container_title | American journal of nephrology |
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| creator | Ecder, Tevfik McFann, Kimberly K. Raynolds, Mary V. Schrier, Robert W. |
| description | Background: Autosomal dominant polycystic kidney disease (ADPKD) shows a variable clinical course suggesting that genetic modifiers might play a role. There are conflicting results about the effect of angiotensin-converting enzyme (ACE) gene polymorphism on the progression of renal failure in ADPKD. Also, the association between ACE gene polymorphism and the occurrence of left ventricular hypertrophy (LVH) has not been investigated in patients with ADPKD. Methods: ACE genotype analysis was performed in 409 Caucasian patients (137 male, 272 female) with ADPKD. Echocardiographic examination was done in 164 of these patients. Results: There were no significant differences between different ACE genotypes regarding renal function, renal volume, urinary protein excretion, blood pressure, the rate of hypertension, the age at diagnosis of hypertension, the rate of LVH and the incidence of end-stage renal disease (ESRD). Conclusion: ACE gene polymorphism does not have a significant effect on the development of ESRD and the prevalence of LVH in patients with ADPKD. |
| doi_str_mv | 10.1159/000074653 |
| format | Article |
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There are conflicting results about the effect of angiotensin-converting enzyme (ACE) gene polymorphism on the progression of renal failure in ADPKD. Also, the association between ACE gene polymorphism and the occurrence of left ventricular hypertrophy (LVH) has not been investigated in patients with ADPKD. Methods: ACE genotype analysis was performed in 409 Caucasian patients (137 male, 272 female) with ADPKD. Echocardiographic examination was done in 164 of these patients. Results: There were no significant differences between different ACE genotypes regarding renal function, renal volume, urinary protein excretion, blood pressure, the rate of hypertension, the age at diagnosis of hypertension, the rate of LVH and the incidence of end-stage renal disease (ESRD). Conclusion: ACE gene polymorphism does not have a significant effect on the development of ESRD and the prevalence of LVH in patients with ADPKD.</description><identifier>ISSN: 0250-8095</identifier><identifier>EISSN: 1421-9670</identifier><identifier>DOI: 10.1159/000074653</identifier><identifier>PMID: 14600431</identifier><identifier>CODEN: AJNED9</identifier><language>eng</language><publisher>Basel, Switzerland: Karger</publisher><subject>Adult ; Age of Onset ; Biological and medical sciences ; Blood Pressure - genetics ; Disease Progression ; European Continental Ancestry Group - genetics ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Humans ; Hypertrophy, Left Ventricular - epidemiology ; Hypertrophy, Left Ventricular - genetics ; Hypertrophy, Left Ventricular - physiopathology ; Kidney Failure, Chronic - epidemiology ; Kidney Failure, Chronic - genetics ; Kidney Failure, Chronic - physiopathology ; Kidney Function Tests ; Kidneys ; Male ; Medical sciences ; Nephrology. Urinary tract diseases ; Original Report: Patient-Oriented, Translational Research ; Peptidyl-Dipeptidase A - genetics ; Polycystic Kidney, Autosomal Dominant - epidemiology ; Polycystic Kidney, Autosomal Dominant - genetics ; Polycystic Kidney, Autosomal Dominant - physiopathology ; Polymorphism, Genetic ; Tumors of the urinary system</subject><ispartof>American journal of nephrology, 2003-11, Vol.23 (6), p.466-470</ispartof><rights>2003 S. Karger AG, Basel</rights><rights>2004 INIST-CNRS</rights><rights>Copyright 2003 S. Karger AG, Basel</rights><rights>Copyright (c) 2003 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c416t-7db3988ced99d9e56dda3faf7d155c8e810a6e86260daabc3f01027f0c9c5fac3</citedby><cites>FETCH-LOGICAL-c416t-7db3988ced99d9e56dda3faf7d155c8e810a6e86260daabc3f01027f0c9c5fac3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,2429,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15304078$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14600431$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ecder, Tevfik</creatorcontrib><creatorcontrib>McFann, Kimberly K.</creatorcontrib><creatorcontrib>Raynolds, Mary V.</creatorcontrib><creatorcontrib>Schrier, Robert W.</creatorcontrib><title>No Effect of Angiotensin-Converting Enzyme Gene Polymorphism on Disease Progression and Left Ventricular Hypertrophy in Autosomal Dominant Polycystic Kidney Disease</title><title>American journal of nephrology</title><addtitle>Am J Nephrol</addtitle><description>Background: Autosomal dominant polycystic kidney disease (ADPKD) shows a variable clinical course suggesting that genetic modifiers might play a role. There are conflicting results about the effect of angiotensin-converting enzyme (ACE) gene polymorphism on the progression of renal failure in ADPKD. Also, the association between ACE gene polymorphism and the occurrence of left ventricular hypertrophy (LVH) has not been investigated in patients with ADPKD. Methods: ACE genotype analysis was performed in 409 Caucasian patients (137 male, 272 female) with ADPKD. Echocardiographic examination was done in 164 of these patients. Results: There were no significant differences between different ACE genotypes regarding renal function, renal volume, urinary protein excretion, blood pressure, the rate of hypertension, the age at diagnosis of hypertension, the rate of LVH and the incidence of end-stage renal disease (ESRD). Conclusion: ACE gene polymorphism does not have a significant effect on the development of ESRD and the prevalence of LVH in patients with ADPKD.</description><subject>Adult</subject><subject>Age of Onset</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - genetics</subject><subject>Disease Progression</subject><subject>European Continental Ancestry Group - genetics</subject><subject>Female</subject><subject>Gene Frequency</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Humans</subject><subject>Hypertrophy, Left Ventricular - epidemiology</subject><subject>Hypertrophy, Left Ventricular - genetics</subject><subject>Hypertrophy, Left Ventricular - physiopathology</subject><subject>Kidney Failure, Chronic - epidemiology</subject><subject>Kidney Failure, Chronic - genetics</subject><subject>Kidney Failure, Chronic - physiopathology</subject><subject>Kidney Function Tests</subject><subject>Kidneys</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Original Report: Patient-Oriented, Translational Research</subject><subject>Peptidyl-Dipeptidase A - genetics</subject><subject>Polycystic Kidney, Autosomal Dominant - epidemiology</subject><subject>Polycystic Kidney, Autosomal Dominant - genetics</subject><subject>Polycystic Kidney, Autosomal Dominant - physiopathology</subject><subject>Polymorphism, Genetic</subject><subject>Tumors of the urinary system</subject><issn>0250-8095</issn><issn>1421-9670</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqF0UGL1DAUB_AiijuuHjwLEgQFD9WXpmmb4zA77qrD6kG9lkzyMpu1TWrSCvXz-EGNO-MOiGAugcePf97Ly7LHFF5RysVrSKcuK87uZAtaFjQXVQ13swUUHPIGBD_JHsR4DUCLBur72QktK4CS0UX289KTtTGoRuINWbqd9SO6aF2-8u47htG6HVm7H3OP5Bwdko--m3sfhisbe-IdObMRZUz14HcBY7SpJp0mGzQj-YJuDFZNnQzkYh5SXPDD1UysI8tp9NH3siNnvrdOuvEmWs1xtIq8t9rh_Cf8YXbPyC7io8N9mn1-s_60usg3H87frpabXJW0GvNab5loGoVaCC2QV1pLZqSpNeVcNdhQkBU2VVGBlnKrmAEKRW1ACcWNVOw0e7HPHYL_NmEc295GhV0nHfoptjVlDeWs_C8saPrhqhQJPvsLXvspuDREWzCoBQfGEnq5Ryr4GAOadgi2l2FuKbS_F9zeLjjZp4fAadujPsrDRhN4fgAyKtmZIJ2y8eg4gxLq5tjZVxl2GG7B8t3lzUvtoE1CT_6J9r38Aj29xLc</recordid><startdate>200311</startdate><enddate>200311</enddate><creator>Ecder, Tevfik</creator><creator>McFann, Kimberly K.</creator><creator>Raynolds, Mary V.</creator><creator>Schrier, Robert W.</creator><general>Karger</general><general>S. 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Urinary tract diseases</topic><topic>Original Report: Patient-Oriented, Translational Research</topic><topic>Peptidyl-Dipeptidase A - genetics</topic><topic>Polycystic Kidney, Autosomal Dominant - epidemiology</topic><topic>Polycystic Kidney, Autosomal Dominant - genetics</topic><topic>Polycystic Kidney, Autosomal Dominant - physiopathology</topic><topic>Polymorphism, Genetic</topic><topic>Tumors of the urinary system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ecder, Tevfik</creatorcontrib><creatorcontrib>McFann, Kimberly K.</creatorcontrib><creatorcontrib>Raynolds, Mary V.</creatorcontrib><creatorcontrib>Schrier, Robert W.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of nephrology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ecder, Tevfik</au><au>McFann, Kimberly K.</au><au>Raynolds, Mary V.</au><au>Schrier, Robert W.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>No Effect of Angiotensin-Converting Enzyme Gene Polymorphism on Disease Progression and Left Ventricular Hypertrophy in Autosomal Dominant Polycystic Kidney Disease</atitle><jtitle>American journal of nephrology</jtitle><addtitle>Am J Nephrol</addtitle><date>2003-11</date><risdate>2003</risdate><volume>23</volume><issue>6</issue><spage>466</spage><epage>470</epage><pages>466-470</pages><issn>0250-8095</issn><eissn>1421-9670</eissn><coden>AJNED9</coden><abstract>Background: Autosomal dominant polycystic kidney disease (ADPKD) shows a variable clinical course suggesting that genetic modifiers might play a role. There are conflicting results about the effect of angiotensin-converting enzyme (ACE) gene polymorphism on the progression of renal failure in ADPKD. Also, the association between ACE gene polymorphism and the occurrence of left ventricular hypertrophy (LVH) has not been investigated in patients with ADPKD. Methods: ACE genotype analysis was performed in 409 Caucasian patients (137 male, 272 female) with ADPKD. Echocardiographic examination was done in 164 of these patients. Results: There were no significant differences between different ACE genotypes regarding renal function, renal volume, urinary protein excretion, blood pressure, the rate of hypertension, the age at diagnosis of hypertension, the rate of LVH and the incidence of end-stage renal disease (ESRD). Conclusion: ACE gene polymorphism does not have a significant effect on the development of ESRD and the prevalence of LVH in patients with ADPKD.</abstract><cop>Basel, Switzerland</cop><pub>Karger</pub><pmid>14600431</pmid><doi>10.1159/000074653</doi><tpages>5</tpages></addata></record> |
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| ispartof | American journal of nephrology, 2003-11, Vol.23 (6), p.466-470 |
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| subjects | Adult Age of Onset Biological and medical sciences Blood Pressure - genetics Disease Progression European Continental Ancestry Group - genetics Female Gene Frequency Genetic Predisposition to Disease Genotype Humans Hypertrophy, Left Ventricular - epidemiology Hypertrophy, Left Ventricular - genetics Hypertrophy, Left Ventricular - physiopathology Kidney Failure, Chronic - epidemiology Kidney Failure, Chronic - genetics Kidney Failure, Chronic - physiopathology Kidney Function Tests Kidneys Male Medical sciences Nephrology. Urinary tract diseases Original Report: Patient-Oriented, Translational Research Peptidyl-Dipeptidase A - genetics Polycystic Kidney, Autosomal Dominant - epidemiology Polycystic Kidney, Autosomal Dominant - genetics Polycystic Kidney, Autosomal Dominant - physiopathology Polymorphism, Genetic Tumors of the urinary system |
| title | No Effect of Angiotensin-Converting Enzyme Gene Polymorphism on Disease Progression and Left Ventricular Hypertrophy in Autosomal Dominant Polycystic Kidney Disease |
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