Variance of ACE and AT1 receptor gene does not influence the risk of neonatal acute renal failure
High neonatal activity of the renin-angiotensin system (RAS) is crucial for the maintenance of glomerular filtration of the newborn. The aim of the present study was to investigate whether genetic polymorphisms leading to lower angiotensin converting enzyme activity (ACE) or impaired functionality o...
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| Veröffentlicht in: | Pediatric nephrology (Berlin, West) West), 2001-12, Vol.16 (12), p.1063-1066 |
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| creator | NOBILIS, Andras KOCSIS, Istvan TOTH-HEYN, Péter TRESZL, Andras SCHULER, Agnes TULASSAY, Tivadar VASARHELYI, Barna |
| description | High neonatal activity of the renin-angiotensin system (RAS) is crucial for the maintenance of glomerular filtration of the newborn. The aim of the present study was to investigate whether genetic polymorphisms leading to lower angiotensin converting enzyme activity (ACE) or impaired functionality of angiotensin II (AII) type 1 receptor (AT1R) might predispose very low birth weight newborns (VLBWs) to the development of acute renal failure (ARF). The medical records of 110 VLBW infants were analyzed. ARF developed in 42 of them during the first postnatal week, while 68 neonates exhibited normal renal function. The ACE I/D polymorphism and the A1166C variants of AT1R were determined from dried blood samples. The frequency of the ACE I allele did not differ in ARF and non-ARF groups (0.307 and 0.284); the frequency of the AT1R C1166 variant was also the same in ARF and non-ARF groups (0.250 and 0.227). Although low activity of RAS has been implicated in the development of neonatal ARF and data indicated that the functionality of RAS is influenced by the I/D variants of the ACE gene and the A1166C variant of the AT1R gene, we could not demonstrate any effect of these polymorphisms on the development of ARF in VLBW infants. |
| doi_str_mv | 10.1007/s004670100028 |
| format | Article |
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The aim of the present study was to investigate whether genetic polymorphisms leading to lower angiotensin converting enzyme activity (ACE) or impaired functionality of angiotensin II (AII) type 1 receptor (AT1R) might predispose very low birth weight newborns (VLBWs) to the development of acute renal failure (ARF). The medical records of 110 VLBW infants were analyzed. ARF developed in 42 of them during the first postnatal week, while 68 neonates exhibited normal renal function. The ACE I/D polymorphism and the A1166C variants of AT1R were determined from dried blood samples. The frequency of the ACE I allele did not differ in ARF and non-ARF groups (0.307 and 0.284); the frequency of the AT1R C1166 variant was also the same in ARF and non-ARF groups (0.250 and 0.227). Although low activity of RAS has been implicated in the development of neonatal ARF and data indicated that the functionality of RAS is influenced by the I/D variants of the ACE gene and the A1166C variant of the AT1R gene, we could not demonstrate any effect of these polymorphisms on the development of ARF in VLBW infants.</description><identifier>ISSN: 0931-041X</identifier><identifier>EISSN: 1432-198X</identifier><identifier>DOI: 10.1007/s004670100028</identifier><identifier>PMID: 11793101</identifier><identifier>CODEN: PENED3</identifier><language>eng</language><publisher>Heidelberg: Springer</publisher><subject>Acute Kidney Injury - etiology ; Acute Kidney Injury - genetics ; Alleles ; Babies ; Biological and medical sciences ; Birth weight ; Blood pressure ; DNA Transposable Elements ; Endocrine system ; Enzymes ; Gene Deletion ; Gene Frequency ; Genetic Predisposition to Disease ; Genetic Variation ; Gynecology ; Humans ; Infant, Newborn ; Intensive care ; Medical records ; Medical sciences ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; Newborn babies ; Obstetrics ; Oliguria ; Peptidyl-Dipeptidase A - genetics ; Polymorphism ; Receptor, Angiotensin, Type 1 ; Receptors, Angiotensin - genetics ; Renal failure ; Respiratory distress syndrome ; Risk Factors ; Sepsis</subject><ispartof>Pediatric nephrology (Berlin, West), 2001-12, Vol.16 (12), p.1063-1066</ispartof><rights>2002 INIST-CNRS</rights><rights>IPNA - International Pediatric Nephrology Association New York, USA 2001</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c346t-22cb6205293918fd575629e0fe6d6e4e16a077a209af06139f2d9faf018c3c3b3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14143706$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11793101$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>NOBILIS, Andras</creatorcontrib><creatorcontrib>KOCSIS, Istvan</creatorcontrib><creatorcontrib>TOTH-HEYN, Péter</creatorcontrib><creatorcontrib>TRESZL, Andras</creatorcontrib><creatorcontrib>SCHULER, Agnes</creatorcontrib><creatorcontrib>TULASSAY, Tivadar</creatorcontrib><creatorcontrib>VASARHELYI, Barna</creatorcontrib><title>Variance of ACE and AT1 receptor gene does not influence the risk of neonatal acute renal failure</title><title>Pediatric nephrology (Berlin, West)</title><addtitle>Pediatr Nephrol</addtitle><description>High neonatal activity of the renin-angiotensin system (RAS) is crucial for the maintenance of glomerular filtration of the newborn. The aim of the present study was to investigate whether genetic polymorphisms leading to lower angiotensin converting enzyme activity (ACE) or impaired functionality of angiotensin II (AII) type 1 receptor (AT1R) might predispose very low birth weight newborns (VLBWs) to the development of acute renal failure (ARF). The medical records of 110 VLBW infants were analyzed. ARF developed in 42 of them during the first postnatal week, while 68 neonates exhibited normal renal function. The ACE I/D polymorphism and the A1166C variants of AT1R were determined from dried blood samples. The frequency of the ACE I allele did not differ in ARF and non-ARF groups (0.307 and 0.284); the frequency of the AT1R C1166 variant was also the same in ARF and non-ARF groups (0.250 and 0.227). Although low activity of RAS has been implicated in the development of neonatal ARF and data indicated that the functionality of RAS is influenced by the I/D variants of the ACE gene and the A1166C variant of the AT1R gene, we could not demonstrate any effect of these polymorphisms on the development of ARF in VLBW infants.</description><subject>Acute Kidney Injury - etiology</subject><subject>Acute Kidney Injury - genetics</subject><subject>Alleles</subject><subject>Babies</subject><subject>Biological and medical sciences</subject><subject>Birth weight</subject><subject>Blood pressure</subject><subject>DNA Transposable Elements</subject><subject>Endocrine system</subject><subject>Enzymes</subject><subject>Gene Deletion</subject><subject>Gene Frequency</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetic Variation</subject><subject>Gynecology</subject><subject>Humans</subject><subject>Infant, Newborn</subject><subject>Intensive care</subject><subject>Medical records</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>Newborn babies</subject><subject>Obstetrics</subject><subject>Oliguria</subject><subject>Peptidyl-Dipeptidase A - genetics</subject><subject>Polymorphism</subject><subject>Receptor, Angiotensin, Type 1</subject><subject>Receptors, Angiotensin - genetics</subject><subject>Renal failure</subject><subject>Respiratory distress syndrome</subject><subject>Risk Factors</subject><subject>Sepsis</subject><issn>0931-041X</issn><issn>1432-198X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpd0c9LwzAUB_Agis7p0asEQW_Vl6RNk-MY8wcMvEzZrWTpi3Z27Uzag_-9GSsMPeWR98nj8Q0hVwzuGUD-EABSmUOsgasjMmKp4AnTanlMRqAFSyBlyzNyHsI6EpUpeUrOGMtjC9iImHfjK9NYpK2jk-mMmqakkwWjHi1uu9bTD2yQli0G2rQdrRpX97jz3SdSX4Wv3cMG28Z0pqbG9l28xibWzlR17_GCnDhTB7wczjF5e5wtps_J_PXpZTqZJ1aksks4tyvJIeNaaKZcmeWZ5BrBoSwlpsikgTw3HLRxIJnQjpfaxZopK6xYiTG528_d-va7x9AVmypYrGsTt-tDkXOhVQYQ4c0_uG57HzcOBedcKKGUiCjZI-vbEDy6YuurjfE_BYNiF3zxJ_jor4eh_WqD5UEPSUdwOwATrKmdj6FX4eDS-HE5SPEL4hOIVw</recordid><startdate>20011201</startdate><enddate>20011201</enddate><creator>NOBILIS, Andras</creator><creator>KOCSIS, Istvan</creator><creator>TOTH-HEYN, Péter</creator><creator>TRESZL, Andras</creator><creator>SCHULER, Agnes</creator><creator>TULASSAY, Tivadar</creator><creator>VASARHELYI, Barna</creator><general>Springer</general><general>Springer Nature B.V</general><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>20011201</creationdate><title>Variance of ACE and AT1 receptor gene does not influence the risk of neonatal acute renal failure</title><author>NOBILIS, Andras ; KOCSIS, Istvan ; TOTH-HEYN, Péter ; TRESZL, Andras ; SCHULER, Agnes ; TULASSAY, Tivadar ; VASARHELYI, Barna</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c346t-22cb6205293918fd575629e0fe6d6e4e16a077a209af06139f2d9faf018c3c3b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Acute Kidney Injury - etiology</topic><topic>Acute Kidney Injury - genetics</topic><topic>Alleles</topic><topic>Babies</topic><topic>Biological and medical sciences</topic><topic>Birth weight</topic><topic>Blood pressure</topic><topic>DNA Transposable Elements</topic><topic>Endocrine system</topic><topic>Enzymes</topic><topic>Gene Deletion</topic><topic>Gene Frequency</topic><topic>Genetic Predisposition to Disease</topic><topic>Genetic Variation</topic><topic>Gynecology</topic><topic>Humans</topic><topic>Infant, Newborn</topic><topic>Intensive care</topic><topic>Medical records</topic><topic>Medical sciences</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>Newborn babies</topic><topic>Obstetrics</topic><topic>Oliguria</topic><topic>Peptidyl-Dipeptidase A - genetics</topic><topic>Polymorphism</topic><topic>Receptor, Angiotensin, Type 1</topic><topic>Receptors, Angiotensin - genetics</topic><topic>Renal failure</topic><topic>Respiratory distress syndrome</topic><topic>Risk Factors</topic><topic>Sepsis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>NOBILIS, Andras</creatorcontrib><creatorcontrib>KOCSIS, Istvan</creatorcontrib><creatorcontrib>TOTH-HEYN, Péter</creatorcontrib><creatorcontrib>TRESZL, Andras</creatorcontrib><creatorcontrib>SCHULER, Agnes</creatorcontrib><creatorcontrib>TULASSAY, Tivadar</creatorcontrib><creatorcontrib>VASARHELYI, Barna</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>Calcium & Calcified Tissue Abstracts</collection><collection>ProQuest Nursing and Allied Health Source</collection><collection>ProQuest Health and Medical</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 UK/Ireland</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</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Family Health</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</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>MEDLINE - Academic</collection><jtitle>Pediatric nephrology (Berlin, West)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>NOBILIS, Andras</au><au>KOCSIS, Istvan</au><au>TOTH-HEYN, Péter</au><au>TRESZL, Andras</au><au>SCHULER, Agnes</au><au>TULASSAY, Tivadar</au><au>VASARHELYI, Barna</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Variance of ACE and AT1 receptor gene does not influence the risk of neonatal acute renal failure</atitle><jtitle>Pediatric nephrology (Berlin, West)</jtitle><addtitle>Pediatr Nephrol</addtitle><date>2001-12-01</date><risdate>2001</risdate><volume>16</volume><issue>12</issue><spage>1063</spage><epage>1066</epage><pages>1063-1066</pages><issn>0931-041X</issn><eissn>1432-198X</eissn><coden>PENED3</coden><abstract>High neonatal activity of the renin-angiotensin system (RAS) is crucial for the maintenance of glomerular filtration of the newborn. The aim of the present study was to investigate whether genetic polymorphisms leading to lower angiotensin converting enzyme activity (ACE) or impaired functionality of angiotensin II (AII) type 1 receptor (AT1R) might predispose very low birth weight newborns (VLBWs) to the development of acute renal failure (ARF). The medical records of 110 VLBW infants were analyzed. ARF developed in 42 of them during the first postnatal week, while 68 neonates exhibited normal renal function. The ACE I/D polymorphism and the A1166C variants of AT1R were determined from dried blood samples. The frequency of the ACE I allele did not differ in ARF and non-ARF groups (0.307 and 0.284); the frequency of the AT1R C1166 variant was also the same in ARF and non-ARF groups (0.250 and 0.227). Although low activity of RAS has been implicated in the development of neonatal ARF and data indicated that the functionality of RAS is influenced by the I/D variants of the ACE gene and the A1166C variant of the AT1R gene, we could not demonstrate any effect of these polymorphisms on the development of ARF in VLBW infants.</abstract><cop>Heidelberg</cop><pub>Springer</pub><pmid>11793101</pmid><doi>10.1007/s004670100028</doi><tpages>4</tpages></addata></record> |
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| ispartof | Pediatric nephrology (Berlin, West), 2001-12, Vol.16 (12), p.1063-1066 |
| issn | 0931-041X 1432-198X |
| language | eng |
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| source | MEDLINE; Springer Nature |
| subjects | Acute Kidney Injury - etiology Acute Kidney Injury - genetics Alleles Babies Biological and medical sciences Birth weight Blood pressure DNA Transposable Elements Endocrine system Enzymes Gene Deletion Gene Frequency Genetic Predisposition to Disease Genetic Variation Gynecology Humans Infant, Newborn Intensive care Medical records Medical sciences Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure Newborn babies Obstetrics Oliguria Peptidyl-Dipeptidase A - genetics Polymorphism Receptor, Angiotensin, Type 1 Receptors, Angiotensin - genetics Renal failure Respiratory distress syndrome Risk Factors Sepsis |
| title | Variance of ACE and AT1 receptor gene does not influence the risk of neonatal acute renal failure |
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