Loading…
ACE and AT1 receptor gene polymorphisms and renal scarring in urinary bladder dysfunction
The objective of this study was to investigate whether DNA polymorphisms of the renin-angiotensin system (RAS) genes were associated with renal scar formation in pediatric patients with bladder dysfunction (BD). Although these children are born healthy, due to persistence of immature voiding habits...
Saved in:
Published in: | Pediatric nephrology (Berlin, West) West), 2004-08, Vol.19 (8), p.853-857 |
---|---|
Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
cited_by | cdi_FETCH-LOGICAL-c324t-2309782f83931ab4754ae0ce2497efc822d2062e25def8ee312a608859467f9e3 |
---|---|
cites | cdi_FETCH-LOGICAL-c324t-2309782f83931ab4754ae0ce2497efc822d2062e25def8ee312a608859467f9e3 |
container_end_page | 857 |
container_issue | 8 |
container_start_page | 853 |
container_title | Pediatric nephrology (Berlin, West) |
container_volume | 19 |
creator | Kostic, Mirjana Stankovic, Aleksandra Zivkovic, Maja Peco-Antic, Amira Jovanovic, Olga Alavantic, Dragan Kruscic, Divna |
description | The objective of this study was to investigate whether DNA polymorphisms of the renin-angiotensin system (RAS) genes were associated with renal scar formation in pediatric patients with bladder dysfunction (BD). Although these children are born healthy, due to persistence of immature voiding habits and evolution of BD, some develop progressive renal damage. It has been suggested that the DD genotype of the angiotensin I-converting enzyme (ACE) gene might be an adverse renal prognostic factor. The insertion/deletion (I/D) polymorphism of the ACE gene and the A1166C polymorphism of the angiotensin II type 1 receptor (ATR1) gene were identified by polymerase chain reaction amplification in 42 children with BD (aged 5-14 years) and 198 healthy adult controls. Twelve children had urgency syndrome and 30 had dysfunctional voiding. Renal scarring was found in 16 patients, while 26 patients had normal kidneys on dimercaptosuccinic acid scan. In children with renal lesions there was significant over-representation of the DD genotype compared with either controls or patients without renal damage ( P |
doi_str_mv | 10.1007/s00467-004-1511-3 |
format | article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_66714296</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1316911811</sourcerecordid><originalsourceid>FETCH-LOGICAL-c324t-2309782f83931ab4754ae0ce2497efc822d2062e25def8ee312a608859467f9e3</originalsourceid><addsrcrecordid>eNpdkEtPwzAQhC0EoqXwA7ggiwO3gF9x7GNVlYdUiUuRyslynU1JlcTBbg7997i0EhKX3T18M9oZhG4peaSEFE-RECGLLM2M5pRm_AyNqeAso1qtztGYaE4zIuhqhK5i3BJCVK7kJRolutC51GP0OZ3Nse1KPF1SHMBBv_MBb6AD3Ptm3_rQf9Wxjb9MgM42ODobQt1tcN3hIR027PG6sWUJAZf7WA2d29W-u0YXlW0i3Jz2BH08z5ez12zx_vI2my4yx5nYZYwTXShWKZ6etWtR5MICccCELqByirGSEcmA5SVUCoBTZiVRKtcpeqWBT9DD0bcP_nuAuDNtHR00je3AD9FIWVDBtEzg_T9w64eQEkXDGOOSa8USRI-QCz7GAJXpQ92miIYScyjdHEs3aZpD6YYnzd3JeFi3UP4pTi3zH5VDe90</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>222363982</pqid></control><display><type>article</type><title>ACE and AT1 receptor gene polymorphisms and renal scarring in urinary bladder dysfunction</title><source>Springer Nature</source><creator>Kostic, Mirjana ; Stankovic, Aleksandra ; Zivkovic, Maja ; Peco-Antic, Amira ; Jovanovic, Olga ; Alavantic, Dragan ; Kruscic, Divna</creator><creatorcontrib>Kostic, Mirjana ; Stankovic, Aleksandra ; Zivkovic, Maja ; Peco-Antic, Amira ; Jovanovic, Olga ; Alavantic, Dragan ; Kruscic, Divna</creatorcontrib><description>The objective of this study was to investigate whether DNA polymorphisms of the renin-angiotensin system (RAS) genes were associated with renal scar formation in pediatric patients with bladder dysfunction (BD). Although these children are born healthy, due to persistence of immature voiding habits and evolution of BD, some develop progressive renal damage. It has been suggested that the DD genotype of the angiotensin I-converting enzyme (ACE) gene might be an adverse renal prognostic factor. The insertion/deletion (I/D) polymorphism of the ACE gene and the A1166C polymorphism of the angiotensin II type 1 receptor (ATR1) gene were identified by polymerase chain reaction amplification in 42 children with BD (aged 5-14 years) and 198 healthy adult controls. Twelve children had urgency syndrome and 30 had dysfunctional voiding. Renal scarring was found in 16 patients, while 26 patients had normal kidneys on dimercaptosuccinic acid scan. In children with renal lesions there was significant over-representation of the DD genotype compared with either controls or patients without renal damage ( P<0.05). On multivariate analysis, the DD genotype was the only factor that had a significant impact on renal scar formation, introducing a 2.51-fold risk (odds ratio 2.51, 95% confidence interval 1.04-6.04, P=0.04). The A1166C gene polymorphism was not significantly associated with the development of parenchymal damage in children with BD. Our findings introduce ACE I/D gene polymorphism as an independent risk factor for parenchymal destruction in pediatric patients with BD.</description><identifier>ISSN: 0931-041X</identifier><identifier>EISSN: 1432-198X</identifier><identifier>DOI: 10.1007/s00467-004-1511-3</identifier><identifier>PMID: 15179569</identifier><language>eng</language><publisher>Germany: Springer Nature B.V</publisher><subject>Adolescent ; Bladder ; Child ; Child, Preschool ; Chronic illnesses ; Cicatrix - etiology ; Cicatrix - genetics ; Congenital diseases ; Creatinine ; Endocrine system ; Enzymes ; Female ; Genes ; Genotype ; Genotype & phenotype ; Humans ; Kidney Diseases - etiology ; Kidney Diseases - genetics ; Kidneys ; Male ; Patients ; Pediatrics ; Peptidyl-Dipeptidase A - genetics ; Polymorphism ; Polymorphism, Genetic ; Prospective Studies ; Receptor, Angiotensin, Type 1 - genetics ; Scars ; Urinary incontinence ; Urinary Incontinence - complications ; Urinary Incontinence - genetics ; Urinary tract infections ; Urogenital system</subject><ispartof>Pediatric nephrology (Berlin, West), 2004-08, Vol.19 (8), p.853-857</ispartof><rights>IPNA 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c324t-2309782f83931ab4754ae0ce2497efc822d2062e25def8ee312a608859467f9e3</citedby><cites>FETCH-LOGICAL-c324t-2309782f83931ab4754ae0ce2497efc822d2062e25def8ee312a608859467f9e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15179569$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kostic, Mirjana</creatorcontrib><creatorcontrib>Stankovic, Aleksandra</creatorcontrib><creatorcontrib>Zivkovic, Maja</creatorcontrib><creatorcontrib>Peco-Antic, Amira</creatorcontrib><creatorcontrib>Jovanovic, Olga</creatorcontrib><creatorcontrib>Alavantic, Dragan</creatorcontrib><creatorcontrib>Kruscic, Divna</creatorcontrib><title>ACE and AT1 receptor gene polymorphisms and renal scarring in urinary bladder dysfunction</title><title>Pediatric nephrology (Berlin, West)</title><addtitle>Pediatr Nephrol</addtitle><description>The objective of this study was to investigate whether DNA polymorphisms of the renin-angiotensin system (RAS) genes were associated with renal scar formation in pediatric patients with bladder dysfunction (BD). Although these children are born healthy, due to persistence of immature voiding habits and evolution of BD, some develop progressive renal damage. It has been suggested that the DD genotype of the angiotensin I-converting enzyme (ACE) gene might be an adverse renal prognostic factor. The insertion/deletion (I/D) polymorphism of the ACE gene and the A1166C polymorphism of the angiotensin II type 1 receptor (ATR1) gene were identified by polymerase chain reaction amplification in 42 children with BD (aged 5-14 years) and 198 healthy adult controls. Twelve children had urgency syndrome and 30 had dysfunctional voiding. Renal scarring was found in 16 patients, while 26 patients had normal kidneys on dimercaptosuccinic acid scan. In children with renal lesions there was significant over-representation of the DD genotype compared with either controls or patients without renal damage ( P<0.05). On multivariate analysis, the DD genotype was the only factor that had a significant impact on renal scar formation, introducing a 2.51-fold risk (odds ratio 2.51, 95% confidence interval 1.04-6.04, P=0.04). The A1166C gene polymorphism was not significantly associated with the development of parenchymal damage in children with BD. Our findings introduce ACE I/D gene polymorphism as an independent risk factor for parenchymal destruction in pediatric patients with BD.</description><subject>Adolescent</subject><subject>Bladder</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Chronic illnesses</subject><subject>Cicatrix - etiology</subject><subject>Cicatrix - genetics</subject><subject>Congenital diseases</subject><subject>Creatinine</subject><subject>Endocrine system</subject><subject>Enzymes</subject><subject>Female</subject><subject>Genes</subject><subject>Genotype</subject><subject>Genotype & phenotype</subject><subject>Humans</subject><subject>Kidney Diseases - etiology</subject><subject>Kidney Diseases - genetics</subject><subject>Kidneys</subject><subject>Male</subject><subject>Patients</subject><subject>Pediatrics</subject><subject>Peptidyl-Dipeptidase A - genetics</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Prospective Studies</subject><subject>Receptor, Angiotensin, Type 1 - genetics</subject><subject>Scars</subject><subject>Urinary incontinence</subject><subject>Urinary Incontinence - complications</subject><subject>Urinary Incontinence - genetics</subject><subject>Urinary tract infections</subject><subject>Urogenital system</subject><issn>0931-041X</issn><issn>1432-198X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNpdkEtPwzAQhC0EoqXwA7ggiwO3gF9x7GNVlYdUiUuRyslynU1JlcTBbg7997i0EhKX3T18M9oZhG4peaSEFE-RECGLLM2M5pRm_AyNqeAso1qtztGYaE4zIuhqhK5i3BJCVK7kJRolutC51GP0OZ3Nse1KPF1SHMBBv_MBb6AD3Ptm3_rQf9Wxjb9MgM42ODobQt1tcN3hIR027PG6sWUJAZf7WA2d29W-u0YXlW0i3Jz2BH08z5ez12zx_vI2my4yx5nYZYwTXShWKZ6etWtR5MICccCELqByirGSEcmA5SVUCoBTZiVRKtcpeqWBT9DD0bcP_nuAuDNtHR00je3AD9FIWVDBtEzg_T9w64eQEkXDGOOSa8USRI-QCz7GAJXpQ92miIYScyjdHEs3aZpD6YYnzd3JeFi3UP4pTi3zH5VDe90</recordid><startdate>20040801</startdate><enddate>20040801</enddate><creator>Kostic, Mirjana</creator><creator>Stankovic, Aleksandra</creator><creator>Zivkovic, Maja</creator><creator>Peco-Antic, Amira</creator><creator>Jovanovic, Olga</creator><creator>Alavantic, Dragan</creator><creator>Kruscic, Divna</creator><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20040801</creationdate><title>ACE and AT1 receptor gene polymorphisms and renal scarring in urinary bladder dysfunction</title><author>Kostic, Mirjana ; Stankovic, Aleksandra ; Zivkovic, Maja ; Peco-Antic, Amira ; Jovanovic, Olga ; Alavantic, Dragan ; Kruscic, Divna</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c324t-2309782f83931ab4754ae0ce2497efc822d2062e25def8ee312a608859467f9e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adolescent</topic><topic>Bladder</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Chronic illnesses</topic><topic>Cicatrix - etiology</topic><topic>Cicatrix - genetics</topic><topic>Congenital diseases</topic><topic>Creatinine</topic><topic>Endocrine system</topic><topic>Enzymes</topic><topic>Female</topic><topic>Genes</topic><topic>Genotype</topic><topic>Genotype & phenotype</topic><topic>Humans</topic><topic>Kidney Diseases - etiology</topic><topic>Kidney Diseases - genetics</topic><topic>Kidneys</topic><topic>Male</topic><topic>Patients</topic><topic>Pediatrics</topic><topic>Peptidyl-Dipeptidase A - genetics</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Prospective Studies</topic><topic>Receptor, Angiotensin, Type 1 - genetics</topic><topic>Scars</topic><topic>Urinary incontinence</topic><topic>Urinary Incontinence - complications</topic><topic>Urinary Incontinence - genetics</topic><topic>Urinary tract infections</topic><topic>Urogenital system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kostic, Mirjana</creatorcontrib><creatorcontrib>Stankovic, Aleksandra</creatorcontrib><creatorcontrib>Zivkovic, Maja</creatorcontrib><creatorcontrib>Peco-Antic, Amira</creatorcontrib><creatorcontrib>Jovanovic, Olga</creatorcontrib><creatorcontrib>Alavantic, Dragan</creatorcontrib><creatorcontrib>Kruscic, Divna</creatorcontrib><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>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</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>MEDLINE - Academic</collection><jtitle>Pediatric nephrology (Berlin, West)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kostic, Mirjana</au><au>Stankovic, Aleksandra</au><au>Zivkovic, Maja</au><au>Peco-Antic, Amira</au><au>Jovanovic, Olga</au><au>Alavantic, Dragan</au><au>Kruscic, Divna</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ACE and AT1 receptor gene polymorphisms and renal scarring in urinary bladder dysfunction</atitle><jtitle>Pediatric nephrology (Berlin, West)</jtitle><addtitle>Pediatr Nephrol</addtitle><date>2004-08-01</date><risdate>2004</risdate><volume>19</volume><issue>8</issue><spage>853</spage><epage>857</epage><pages>853-857</pages><issn>0931-041X</issn><eissn>1432-198X</eissn><abstract>The objective of this study was to investigate whether DNA polymorphisms of the renin-angiotensin system (RAS) genes were associated with renal scar formation in pediatric patients with bladder dysfunction (BD). Although these children are born healthy, due to persistence of immature voiding habits and evolution of BD, some develop progressive renal damage. It has been suggested that the DD genotype of the angiotensin I-converting enzyme (ACE) gene might be an adverse renal prognostic factor. The insertion/deletion (I/D) polymorphism of the ACE gene and the A1166C polymorphism of the angiotensin II type 1 receptor (ATR1) gene were identified by polymerase chain reaction amplification in 42 children with BD (aged 5-14 years) and 198 healthy adult controls. Twelve children had urgency syndrome and 30 had dysfunctional voiding. Renal scarring was found in 16 patients, while 26 patients had normal kidneys on dimercaptosuccinic acid scan. In children with renal lesions there was significant over-representation of the DD genotype compared with either controls or patients without renal damage ( P<0.05). On multivariate analysis, the DD genotype was the only factor that had a significant impact on renal scar formation, introducing a 2.51-fold risk (odds ratio 2.51, 95% confidence interval 1.04-6.04, P=0.04). The A1166C gene polymorphism was not significantly associated with the development of parenchymal damage in children with BD. Our findings introduce ACE I/D gene polymorphism as an independent risk factor for parenchymal destruction in pediatric patients with BD.</abstract><cop>Germany</cop><pub>Springer Nature B.V</pub><pmid>15179569</pmid><doi>10.1007/s00467-004-1511-3</doi><tpages>5</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0931-041X |
ispartof | Pediatric nephrology (Berlin, West), 2004-08, Vol.19 (8), p.853-857 |
issn | 0931-041X 1432-198X |
language | eng |
recordid | cdi_proquest_miscellaneous_66714296 |
source | Springer Nature |
subjects | Adolescent Bladder Child Child, Preschool Chronic illnesses Cicatrix - etiology Cicatrix - genetics Congenital diseases Creatinine Endocrine system Enzymes Female Genes Genotype Genotype & phenotype Humans Kidney Diseases - etiology Kidney Diseases - genetics Kidneys Male Patients Pediatrics Peptidyl-Dipeptidase A - genetics Polymorphism Polymorphism, Genetic Prospective Studies Receptor, Angiotensin, Type 1 - genetics Scars Urinary incontinence Urinary Incontinence - complications Urinary Incontinence - genetics Urinary tract infections Urogenital system |
title | ACE and AT1 receptor gene polymorphisms and renal scarring in urinary bladder dysfunction |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-22T17%3A08%3A53IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=ACE%20and%20AT1%20receptor%20gene%20polymorphisms%20and%20renal%20scarring%20in%20urinary%20bladder%20dysfunction&rft.jtitle=Pediatric%20nephrology%20(Berlin,%20West)&rft.au=Kostic,%20Mirjana&rft.date=2004-08-01&rft.volume=19&rft.issue=8&rft.spage=853&rft.epage=857&rft.pages=853-857&rft.issn=0931-041X&rft.eissn=1432-198X&rft_id=info:doi/10.1007/s00467-004-1511-3&rft_dat=%3Cproquest_cross%3E1316911811%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c324t-2309782f83931ab4754ae0ce2497efc822d2062e25def8ee312a608859467f9e3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=222363982&rft_id=info:pmid/15179569&rfr_iscdi=true |