Autosomal dominant hemolytic uremic syndrome: variable phenotypes and transplant results
Autosomal dominant hemolytic uremic syndrome (ADHUS) is a rare disorder with a poor prognosis that was considered to present mainly in adults. Recurrent episodes of ADHUS were also thought to be uncommon. However, increasing reports suggest that children are often affected, that recurrent episodes m...
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Veröffentlicht in: | Pediatric nephrology (Berlin, West) West), 2000-06, Vol.14 (6), p.464-468 |
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description | Autosomal dominant hemolytic uremic syndrome (ADHUS) is a rare disorder with a poor prognosis that was considered to present mainly in adults. Recurrent episodes of ADHUS were also thought to be uncommon. However, increasing reports suggest that children are often affected, that recurrent episodes may occur pretransplantation, and that post-transplant recurrences occur in about 50% of cases. We describe the occurrence of ADHUS in two unrelated families with different outcomes. It is apparent that there are several types of ADHUS (with and without serum complement abnormalities) and that there may be variable expression of the phenotype. There was variable penetration of HUS in four (possibly five) adults and two children in four generations of one kindred. There was also one definite unaffected carrier. Two patients had successful renal transplants without recurrences; the HUS recurred in a third patient soon after transplantation. In a second family, the father had three episodes of HUS at 18, 26 and 29 years of age; his son had one episode of HUS at 5 years of age. Both recovered completely. Evaluation of these patients, previous reports, and follow-up contacts of previous reports suggests that post-transplant recurrence of ADHUS is more common than previously reported and may not be prevented by prior nephrectomy of native kidneys. |
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Recurrent episodes of ADHUS were also thought to be uncommon. However, increasing reports suggest that children are often affected, that recurrent episodes may occur pretransplantation, and that post-transplant recurrences occur in about 50% of cases. We describe the occurrence of ADHUS in two unrelated families with different outcomes. It is apparent that there are several types of ADHUS (with and without serum complement abnormalities) and that there may be variable expression of the phenotype. There was variable penetration of HUS in four (possibly five) adults and two children in four generations of one kindred. There was also one definite unaffected carrier. Two patients had successful renal transplants without recurrences; the HUS recurred in a third patient soon after transplantation. In a second family, the father had three episodes of HUS at 18, 26 and 29 years of age; his son had one episode of HUS at 5 years of age. Both recovered completely. Evaluation of these patients, previous reports, and follow-up contacts of previous reports suggests that post-transplant recurrence of ADHUS is more common than previously reported and may not be prevented by prior nephrectomy of native kidneys.</description><identifier>ISSN: 0931-041X</identifier><identifier>EISSN: 1432-198X</identifier><identifier>DOI: 10.1007/s004670050793</identifier><identifier>PMID: 10872184</identifier><language>eng</language><publisher>Germany: Springer Nature B.V</publisher><subject>Adult ; Aged ; Female ; Genes, Dominant ; Hemolytic-Uremic Syndrome - genetics ; Hemolytic-Uremic Syndrome - therapy ; Humans ; Infant ; Kidney Transplantation - physiology ; Male ; Nephrectomy ; Pedigree ; Phenotype</subject><ispartof>Pediatric nephrology (Berlin, West), 2000-06, Vol.14 (6), p.464-468</ispartof><rights>IPNA - International Pediatric Nephrology Association New York, USA 2000</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c316t-bc6c493c85132447a58b04b375dd54609b351c8542ff0f787d71a5a2e91e5dc33</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10872184$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kaplan, B S</creatorcontrib><creatorcontrib>Leonard, M B</creatorcontrib><title>Autosomal dominant hemolytic uremic syndrome: variable phenotypes and transplant results</title><title>Pediatric nephrology (Berlin, West)</title><addtitle>Pediatr Nephrol</addtitle><description>Autosomal dominant hemolytic uremic syndrome (ADHUS) is a rare disorder with a poor prognosis that was considered to present mainly in adults. 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Evaluation of these patients, previous reports, and follow-up contacts of previous reports suggests that post-transplant recurrence of ADHUS is more common than previously reported and may not be prevented by prior nephrectomy of native kidneys.</description><subject>Adult</subject><subject>Aged</subject><subject>Female</subject><subject>Genes, Dominant</subject><subject>Hemolytic-Uremic Syndrome - genetics</subject><subject>Hemolytic-Uremic Syndrome - therapy</subject><subject>Humans</subject><subject>Infant</subject><subject>Kidney Transplantation - physiology</subject><subject>Male</subject><subject>Nephrectomy</subject><subject>Pedigree</subject><subject>Phenotype</subject><issn>0931-041X</issn><issn>1432-198X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpdkDtPwzAUhS0EoqUwsqKIgS1w_YpjtqriJVViAalb5MSOmiqOg-0g5d-Tqh2A6Qz3u0dHH0LXGO4xgHgIACwTAByEpCdojhklKZb55hTNQVKcAsObGboIYQcAOc-zczTDkAuCczZHm-UQXXBWtYl2tulUF5Otsa4dY1Mlgzd2ijB22jtrHpNv5RtVtibpt6ZzcexNSFSnk-hVF_p2_-1NGNoYLtFZrdpgro65QJ_PTx-r13T9_vK2Wq7TiuIspmWVVUzSKueYEsaE4nkJrKSCa81ZBrKkHE9XRuoaapELLbDiihiJDdcVpQt0d-jtvfsaTIiFbUJl2mmLcUMoBCYEUwkTePsP3LnBd9O2ghBCOZGcT1B6gCrvQvCmLnrfWOXHAkOx91388T3xN8fSobRG_6IPgukPLyB7NQ</recordid><startdate>20000601</startdate><enddate>20000601</enddate><creator>Kaplan, B S</creator><creator>Leonard, M B</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>20000601</creationdate><title>Autosomal dominant hemolytic uremic syndrome: variable phenotypes and transplant results</title><author>Kaplan, B S ; Leonard, M B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c316t-bc6c493c85132447a58b04b375dd54609b351c8542ff0f787d71a5a2e91e5dc33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Female</topic><topic>Genes, Dominant</topic><topic>Hemolytic-Uremic Syndrome - genetics</topic><topic>Hemolytic-Uremic Syndrome - therapy</topic><topic>Humans</topic><topic>Infant</topic><topic>Kidney Transplantation - physiology</topic><topic>Male</topic><topic>Nephrectomy</topic><topic>Pedigree</topic><topic>Phenotype</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kaplan, B S</creatorcontrib><creatorcontrib>Leonard, M B</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 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>Kaplan, B S</au><au>Leonard, M B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Autosomal dominant hemolytic uremic syndrome: variable phenotypes and transplant results</atitle><jtitle>Pediatric nephrology (Berlin, West)</jtitle><addtitle>Pediatr Nephrol</addtitle><date>2000-06-01</date><risdate>2000</risdate><volume>14</volume><issue>6</issue><spage>464</spage><epage>468</epage><pages>464-468</pages><issn>0931-041X</issn><eissn>1432-198X</eissn><abstract>Autosomal dominant hemolytic uremic syndrome (ADHUS) is a rare disorder with a poor prognosis that was considered to present mainly in adults. Recurrent episodes of ADHUS were also thought to be uncommon. However, increasing reports suggest that children are often affected, that recurrent episodes may occur pretransplantation, and that post-transplant recurrences occur in about 50% of cases. We describe the occurrence of ADHUS in two unrelated families with different outcomes. It is apparent that there are several types of ADHUS (with and without serum complement abnormalities) and that there may be variable expression of the phenotype. There was variable penetration of HUS in four (possibly five) adults and two children in four generations of one kindred. There was also one definite unaffected carrier. Two patients had successful renal transplants without recurrences; the HUS recurred in a third patient soon after transplantation. In a second family, the father had three episodes of HUS at 18, 26 and 29 years of age; his son had one episode of HUS at 5 years of age. Both recovered completely. Evaluation of these patients, previous reports, and follow-up contacts of previous reports suggests that post-transplant recurrence of ADHUS is more common than previously reported and may not be prevented by prior nephrectomy of native kidneys.</abstract><cop>Germany</cop><pub>Springer Nature B.V</pub><pmid>10872184</pmid><doi>10.1007/s004670050793</doi><tpages>5</tpages></addata></record> |
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subjects | Adult Aged Female Genes, Dominant Hemolytic-Uremic Syndrome - genetics Hemolytic-Uremic Syndrome - therapy Humans Infant Kidney Transplantation - physiology Male Nephrectomy Pedigree Phenotype |
title | Autosomal dominant hemolytic uremic syndrome: variable phenotypes and transplant results |
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