Renal failure in the neonate associated with in utero exposure to non-steroidal anti-inflammatory agents
In utero exposure to non-steroidal anti-inflammatory agents (NSAIAs) can produce combinations of oligohydramnios, a bleeding diathesis, ileal perforation, premature closure of the ductus, and acute or chronic renal injury. NSAIAs induce renal dysgenesis in fetal monkeys and renal structural abnormal...
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Veröffentlicht in: | Pediatric nephrology (Berlin, West) West), 1994-12, Vol.8 (6), p.700-704 |
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creator | KAPLAN, B. S RESTAINO, I RAVAL, D. S GOTTLIEB, R. P BERNSTEIN, J |
description | In utero exposure to non-steroidal anti-inflammatory agents (NSAIAs) can produce combinations of oligohydramnios, a bleeding diathesis, ileal perforation, premature closure of the ductus, and acute or chronic renal injury. NSAIAs induce renal dysgenesis in fetal monkeys and renal structural abnormalities in the developing human fetus. We report oligohydramnios and renal failure associated with in utero exposure to early, prolonged, high-dose indomethacin in four neonates, and to ibuprofen in one neonate. Four of the affected neonates were one of twins. In each set of twins, only one of the pair was affected. One set of twins was proven to be identical, whereas the other three sets seemed to be identical. It is possible that the histopathological findings of uncertain or incomplete tubular differentiation may be the result of a direct effect of NSAIAs on developing or "immature" tubules. Therefore, the advantages of NSAIAs as tocolytics need to be weighed against the complication of severe renal injury. |
doi_str_mv | 10.1007/BF00869093 |
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In each set of twins, only one of the pair was affected. One set of twins was proven to be identical, whereas the other three sets seemed to be identical. It is possible that the histopathological findings of uncertain or incomplete tubular differentiation may be the result of a direct effect of NSAIAs on developing or "immature" tubules. Therefore, the advantages of NSAIAs as tocolytics need to be weighed against the complication of severe renal injury.</description><subject>Acute Kidney Injury - chemically induced</subject><subject>Acute Kidney Injury - pathology</subject><subject>Adult</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - adverse effects</subject><subject>Biological and medical sciences</subject><subject>Diseases of mother, fetus and pregnancy</subject><subject>Fatal Outcome</subject><subject>Female</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Infant, Newborn</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Pregnancy</subject><subject>Pregnancy. Fetus. Placenta</subject><subject>Prenatal Exposure Delayed Effects</subject><issn>0931-041X</issn><issn>1432-198X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkEFLAzEQhYMotVYv3oUcPAmrySbNJkctVoWCIAq9LZNsYiPbpGxStP_eXVr0NMN73zyYh9AlJbeUkOruYU6IFIoodoTGlLOyoEouj9G4V2hBOF2eorOUvkiPTaUYoVEllKBEjtHqzQZosQPfbjuLfcB5ZXGwMUC2GFKKxvdbg799Xg32NtsuYvuziWk4yBGHGIo0qL7pkyBkX_jgWlivIcduh-HThpzO0YmDNtmLw5ygj_nj--y5WLw-vczuF4UpS5ELqbgzVMtGWA3aKk2YKxswVmiuCWjBiWTKWSLtlDdGOceh7H-vhGlkWQk2QTf7XNPFlDrr6k3n19Dtakrqoa36v60evtrDm61e2-YPPdTT-9cHH5KB1nUQjE9_GGNclJKxXwnmc_M</recordid><startdate>199412</startdate><enddate>199412</enddate><creator>KAPLAN, B. 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P ; BERNSTEIN, J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c226t-894fc1b8d6ebabe9b03f2dace6b4b0ab640839fe08e54dc9ff4a286976cd82763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>Acute Kidney Injury - chemically induced</topic><topic>Acute Kidney Injury - pathology</topic><topic>Adult</topic><topic>Anti-Inflammatory Agents, Non-Steroidal - adverse effects</topic><topic>Biological and medical sciences</topic><topic>Diseases of mother, fetus and pregnancy</topic><topic>Fatal Outcome</topic><topic>Female</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Infant, Newborn</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Pregnancy</topic><topic>Pregnancy. Fetus. Placenta</topic><topic>Prenatal Exposure Delayed Effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>KAPLAN, B. S</creatorcontrib><creatorcontrib>RESTAINO, I</creatorcontrib><creatorcontrib>RAVAL, D. S</creatorcontrib><creatorcontrib>GOTTLIEB, R. P</creatorcontrib><creatorcontrib>BERNSTEIN, J</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><jtitle>Pediatric nephrology (Berlin, West)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KAPLAN, B. S</au><au>RESTAINO, I</au><au>RAVAL, D. S</au><au>GOTTLIEB, R. P</au><au>BERNSTEIN, J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Renal failure in the neonate associated with in utero exposure to non-steroidal anti-inflammatory agents</atitle><jtitle>Pediatric nephrology (Berlin, West)</jtitle><addtitle>Pediatr Nephrol</addtitle><date>1994-12</date><risdate>1994</risdate><volume>8</volume><issue>6</issue><spage>700</spage><epage>704</epage><pages>700-704</pages><issn>0931-041X</issn><eissn>1432-198X</eissn><coden>PENED3</coden><abstract>In utero exposure to non-steroidal anti-inflammatory agents (NSAIAs) can produce combinations of oligohydramnios, a bleeding diathesis, ileal perforation, premature closure of the ductus, and acute or chronic renal injury. NSAIAs induce renal dysgenesis in fetal monkeys and renal structural abnormalities in the developing human fetus. We report oligohydramnios and renal failure associated with in utero exposure to early, prolonged, high-dose indomethacin in four neonates, and to ibuprofen in one neonate. Four of the affected neonates were one of twins. In each set of twins, only one of the pair was affected. One set of twins was proven to be identical, whereas the other three sets seemed to be identical. It is possible that the histopathological findings of uncertain or incomplete tubular differentiation may be the result of a direct effect of NSAIAs on developing or "immature" tubules. Therefore, the advantages of NSAIAs as tocolytics need to be weighed against the complication of severe renal injury.</abstract><cop>Heidelberg</cop><pub>Springer</pub><pmid>7696108</pmid><doi>10.1007/BF00869093</doi><tpages>5</tpages></addata></record> |
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subjects | Acute Kidney Injury - chemically induced Acute Kidney Injury - pathology Adult Anti-Inflammatory Agents, Non-Steroidal - adverse effects Biological and medical sciences Diseases of mother, fetus and pregnancy Fatal Outcome Female Gynecology. Andrology. Obstetrics Humans Infant, Newborn Male Medical sciences Pregnancy Pregnancy. Fetus. Placenta Prenatal Exposure Delayed Effects |
title | Renal failure in the neonate associated with in utero exposure to non-steroidal anti-inflammatory agents |
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