Interleukin genetic variants and the risk of renal failure in infants with infection
Systemic infection is a major risk factor for the development of neonatal acute renal failure (ARF). We investigated whether genetic polymorphisms of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, and IL-10 genes leading to a more intense inflammatory response might predispose very...
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| Veröffentlicht in: | Pediatric nephrology (Berlin, West) West), 2002-09, Vol.17 (9), p.713-717 |
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| container_title | Pediatric nephrology (Berlin, West) |
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| creator | TRESZL, Andras TOTH-HEYN, Péter KOCSIS, Istvan NOBILIS, Andras SCHULER, Agnes TULASSAY, Tivadar VASARHELYI, Barna |
| description | Systemic infection is a major risk factor for the development of neonatal acute renal failure (ARF). We investigated whether genetic polymorphisms of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, and IL-10 genes leading to a more intense inflammatory response might predispose very low birth weight (VLBW) infants to the development of ARF in severe infection. The medical records of 92 VLBW newborns (birth weight under 1,500 g) with systemic infection were analyzed. ARF developed in 38 infants during the 1st postnatal week, while 54 neonates exhibited normal renal function. The variants of TNF-alpha, IL-1beta, IL-6, and IL-10 genes were determined from dried blood samples with polymerase chain reaction and restriction fragment length polymorphism methods. The allele frequencies did not differ in ARF and in non-ARF babies, while the (TNF-alpha /IL-6) AG/GC or AG/CC haplotypes were more often present in ARF (26% vs. 6%, P |
| doi_str_mv | 10.1007/s00467-002-0935-x |
| format | Article |
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We investigated whether genetic polymorphisms of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, and IL-10 genes leading to a more intense inflammatory response might predispose very low birth weight (VLBW) infants to the development of ARF in severe infection. The medical records of 92 VLBW newborns (birth weight under 1,500 g) with systemic infection were analyzed. ARF developed in 38 infants during the 1st postnatal week, while 54 neonates exhibited normal renal function. The variants of TNF-alpha, IL-1beta, IL-6, and IL-10 genes were determined from dried blood samples with polymerase chain reaction and restriction fragment length polymorphism methods. The allele frequencies did not differ in ARF and in non-ARF babies, while the (TNF-alpha /IL-6) AG/GC or AG/CC haplotypes were more often present in ARF (26% vs. 6%, P<0.01). The single presence of TNF-alpha, IL-1beta, IL-6, and IL-10 variants does not influence the development of ARF, but the constellation of TNF-alpha and IL-6 genetic variants is associated with ARF. We hypothesize that the simultaneous presence of these polymorphisms might lead to an enhanced inflammatory response in the kidneys in babies with infection.</description><identifier>ISSN: 0931-041X</identifier><identifier>EISSN: 1432-198X</identifier><identifier>DOI: 10.1007/s00467-002-0935-x</identifier><identifier>PMID: 12215823</identifier><identifier>CODEN: PENED3</identifier><language>eng</language><publisher>Heidelberg: Springer</publisher><subject>Acute Kidney Injury - etiology ; Anemia ; Babies ; Biological and medical sciences ; Birth weight ; Cytokines ; Genetic Variation ; Gynecology ; Humans ; Infant, Newborn ; Infection - complications ; Infections ; Influence ; Interleukin-1 - genetics ; Interleukin-10 - genetics ; Interleukin-6 - genetics ; Interleukins - genetics ; Lung diseases ; Medical records ; Medical sciences ; Metabolism ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; Obstetrics ; Oliguria ; Pediatrics ; Polymerase chain reaction ; Polymorphism ; Polymorphism, Genetic ; Renal failure ; Respiratory distress syndrome ; Risk Factors ; Sepsis ; Tumor Necrosis Factor-alpha - genetics ; Tumor necrosis factor-TNF</subject><ispartof>Pediatric nephrology (Berlin, West), 2002-09, Vol.17 (9), p.713-717</ispartof><rights>2002 INIST-CNRS</rights><rights>IPNA 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c354t-c3883ed5330794e64ba270e0989819ed8309d724f5c9da73427fc51ab57800113</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13918211$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12215823$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>TRESZL, Andras</creatorcontrib><creatorcontrib>TOTH-HEYN, Péter</creatorcontrib><creatorcontrib>KOCSIS, Istvan</creatorcontrib><creatorcontrib>NOBILIS, Andras</creatorcontrib><creatorcontrib>SCHULER, Agnes</creatorcontrib><creatorcontrib>TULASSAY, Tivadar</creatorcontrib><creatorcontrib>VASARHELYI, Barna</creatorcontrib><title>Interleukin genetic variants and the risk of renal failure in infants with infection</title><title>Pediatric nephrology (Berlin, West)</title><addtitle>Pediatr Nephrol</addtitle><description>Systemic infection is a major risk factor for the development of neonatal acute renal failure (ARF). We investigated whether genetic polymorphisms of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, and IL-10 genes leading to a more intense inflammatory response might predispose very low birth weight (VLBW) infants to the development of ARF in severe infection. The medical records of 92 VLBW newborns (birth weight under 1,500 g) with systemic infection were analyzed. ARF developed in 38 infants during the 1st postnatal week, while 54 neonates exhibited normal renal function. The variants of TNF-alpha, IL-1beta, IL-6, and IL-10 genes were determined from dried blood samples with polymerase chain reaction and restriction fragment length polymorphism methods. The allele frequencies did not differ in ARF and in non-ARF babies, while the (TNF-alpha /IL-6) AG/GC or AG/CC haplotypes were more often present in ARF (26% vs. 6%, P<0.01). The single presence of TNF-alpha, IL-1beta, IL-6, and IL-10 variants does not influence the development of ARF, but the constellation of TNF-alpha and IL-6 genetic variants is associated with ARF. We hypothesize that the simultaneous presence of these polymorphisms might lead to an enhanced inflammatory response in the kidneys in babies with infection.</description><subject>Acute Kidney Injury - etiology</subject><subject>Anemia</subject><subject>Babies</subject><subject>Biological and medical sciences</subject><subject>Birth weight</subject><subject>Cytokines</subject><subject>Genetic Variation</subject><subject>Gynecology</subject><subject>Humans</subject><subject>Infant, Newborn</subject><subject>Infection - complications</subject><subject>Infections</subject><subject>Influence</subject><subject>Interleukin-1 - genetics</subject><subject>Interleukin-10 - genetics</subject><subject>Interleukin-6 - genetics</subject><subject>Interleukins - genetics</subject><subject>Lung diseases</subject><subject>Medical records</subject><subject>Medical sciences</subject><subject>Metabolism</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>Obstetrics</subject><subject>Oliguria</subject><subject>Pediatrics</subject><subject>Polymerase chain reaction</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Renal failure</subject><subject>Respiratory distress syndrome</subject><subject>Risk Factors</subject><subject>Sepsis</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor necrosis factor-TNF</subject><issn>0931-041X</issn><issn>1432-198X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpdkMtKBDEQRYMoOj4-wI0EQXetlaQzSZYivkBwo-AuZNLVGu1Ja9Lt4-_NOAOCWVSo4tyCOoTsMzhhAOo0A9RTVQHwCoyQ1dcambBa8IoZ_bhOJmXIKqjZ4xbZzvkFALTU002yxThnUnMxIfc3ccDU4fgaIn3CiEPw9MOl4OKQqYsNHZ6RppBfad_ShNF1tHWhGxPSkgix_QU_w_C8aNAPoY-7ZKN1Xca91b9DHi4v7s-vq9u7q5vzs9vKC1kPpWotsJFCgDI1TuuZ4woQjDaaGWy0ANMoXrfSm8YpUXPVesncTCoNwJjYIcfLvW-pfx8xD3YesseucxH7MVvFYaqVlAU8_Ae-9GMqt2TLy9NScCgQW0I-9TknbO1bCnOXvi0Du_Btl75t8W0Xvu1XyRysFo-zOTZ_iZXgAhytAJe969rkog_5jxOGaV5O-QHYBIcu</recordid><startdate>20020901</startdate><enddate>20020901</enddate><creator>TRESZL, Andras</creator><creator>TOTH-HEYN, Péter</creator><creator>KOCSIS, Istvan</creator><creator>NOBILIS, 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>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20020901</creationdate><title>Interleukin genetic variants and the risk of renal failure in infants with infection</title><author>TRESZL, Andras ; TOTH-HEYN, Péter ; KOCSIS, Istvan ; NOBILIS, Andras ; SCHULER, Agnes ; TULASSAY, Tivadar ; VASARHELYI, Barna</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c354t-c3883ed5330794e64ba270e0989819ed8309d724f5c9da73427fc51ab57800113</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Acute Kidney Injury - etiology</topic><topic>Anemia</topic><topic>Babies</topic><topic>Biological and medical sciences</topic><topic>Birth weight</topic><topic>Cytokines</topic><topic>Genetic Variation</topic><topic>Gynecology</topic><topic>Humans</topic><topic>Infant, Newborn</topic><topic>Infection - complications</topic><topic>Infections</topic><topic>Influence</topic><topic>Interleukin-1 - genetics</topic><topic>Interleukin-10 - genetics</topic><topic>Interleukin-6 - genetics</topic><topic>Interleukins - genetics</topic><topic>Lung diseases</topic><topic>Medical records</topic><topic>Medical sciences</topic><topic>Metabolism</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>Obstetrics</topic><topic>Oliguria</topic><topic>Pediatrics</topic><topic>Polymerase chain reaction</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Renal failure</topic><topic>Respiratory distress syndrome</topic><topic>Risk Factors</topic><topic>Sepsis</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>TRESZL, Andras</creatorcontrib><creatorcontrib>TOTH-HEYN, Péter</creatorcontrib><creatorcontrib>KOCSIS, Istvan</creatorcontrib><creatorcontrib>NOBILIS, 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>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 Edition)</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 (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>TRESZL, Andras</au><au>TOTH-HEYN, Péter</au><au>KOCSIS, Istvan</au><au>NOBILIS, Andras</au><au>SCHULER, Agnes</au><au>TULASSAY, Tivadar</au><au>VASARHELYI, Barna</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interleukin genetic variants and the risk of renal failure in infants with infection</atitle><jtitle>Pediatric nephrology (Berlin, West)</jtitle><addtitle>Pediatr Nephrol</addtitle><date>2002-09-01</date><risdate>2002</risdate><volume>17</volume><issue>9</issue><spage>713</spage><epage>717</epage><pages>713-717</pages><issn>0931-041X</issn><eissn>1432-198X</eissn><coden>PENED3</coden><abstract>Systemic infection is a major risk factor for the development of neonatal acute renal failure (ARF). We investigated whether genetic polymorphisms of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, and IL-10 genes leading to a more intense inflammatory response might predispose very low birth weight (VLBW) infants to the development of ARF in severe infection. The medical records of 92 VLBW newborns (birth weight under 1,500 g) with systemic infection were analyzed. ARF developed in 38 infants during the 1st postnatal week, while 54 neonates exhibited normal renal function. The variants of TNF-alpha, IL-1beta, IL-6, and IL-10 genes were determined from dried blood samples with polymerase chain reaction and restriction fragment length polymorphism methods. The allele frequencies did not differ in ARF and in non-ARF babies, while the (TNF-alpha /IL-6) AG/GC or AG/CC haplotypes were more often present in ARF (26% vs. 6%, P<0.01). The single presence of TNF-alpha, IL-1beta, IL-6, and IL-10 variants does not influence the development of ARF, but the constellation of TNF-alpha and IL-6 genetic variants is associated with ARF. We hypothesize that the simultaneous presence of these polymorphisms might lead to an enhanced inflammatory response in the kidneys in babies with infection.</abstract><cop>Heidelberg</cop><pub>Springer</pub><pmid>12215823</pmid><doi>10.1007/s00467-002-0935-x</doi><tpages>5</tpages></addata></record> |
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| subjects | Acute Kidney Injury - etiology Anemia Babies Biological and medical sciences Birth weight Cytokines Genetic Variation Gynecology Humans Infant, Newborn Infection - complications Infections Influence Interleukin-1 - genetics Interleukin-10 - genetics Interleukin-6 - genetics Interleukins - genetics Lung diseases Medical records Medical sciences Metabolism Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure Obstetrics Oliguria Pediatrics Polymerase chain reaction Polymorphism Polymorphism, Genetic Renal failure Respiratory distress syndrome Risk Factors Sepsis Tumor Necrosis Factor-alpha - genetics Tumor necrosis factor-TNF |
| title | Interleukin genetic variants and the risk of renal failure in infants with infection |
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