Atypical hemolytic uremic syndrome in a patient with protein-losing enteropathy
Atypical hemolytic uremic syndrome (aHUS) is an ultra-rare disease induced by many triggers, all of which produce a common end phenotype of microangiopathic hemolysis and thrombotic microangiopathy. We herein describe a 63-year-old woman with ongoing protein-losing enteropathy and frequent transudat...
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Published in | Journal of international medical research Vol. 47; no. 8; pp. 4027 - 4032 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
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London, England
SAGE Publications
01.08.2019
Sage Publications Ltd SAGE Publishing |
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Abstract | Atypical hemolytic uremic syndrome (aHUS) is an ultra-rare disease induced by many triggers, all of which produce a common end phenotype of microangiopathic hemolysis and thrombotic microangiopathy. We herein describe a 63-year-old woman with ongoing protein-losing enteropathy and frequent transudates caused by hypoalbuminemia. The patient was treated with eculizumab with a full hematologic and partial renal response. Protein-losing enteropathy is an inflammatory condition that has been linked with increased complement activation, which can trigger aHUS in patients with loss of CD55 expression. The patient in the present case had an increased estimated glomerular filtration rate but stage IV to V chronic kidney disease. One year later, she remains off dialysis with a stable estimated glomerular filtration rate. We herein report an unusual trigger of complement activation that in turn triggered aHUS in this patient. |
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AbstractList | Atypical hemolytic uremic syndrome (aHUS) is an ultra-rare disease induced by many triggers, all of which produce a common end phenotype of microangiopathic hemolysis and thrombotic microangiopathy. We herein describe a 63-year-old woman with ongoing protein-losing enteropathy and frequent transudates caused by hypoalbuminemia. The patient was treated with eculizumab with a full hematologic and partial renal response. Protein-losing enteropathy is an inflammatory condition that has been linked with increased complement activation, which can trigger aHUS in patients with loss of CD55 expression. The patient in the present case had an increased estimated glomerular filtration rate but stage IV to V chronic kidney disease. One year later, she remains off dialysis with a stable estimated glomerular filtration rate. We herein report an unusual trigger of complement activation that in turn triggered aHUS in this patient. |
Author | Abdelnour, Lama Hasnain, Huma Hanna, Ramy M. Burwick, Richard M. Yanny, Beshoy |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31364428$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.1056/NEJMra1312353 10.3389/fimmu.2019.00337 10.1182/blood-2017-02-770214 10.1093/qjmed/hcv082 10.1371/journal.pone.0010208 10.1053/j.ajkd.2014.01.434 10.1681/ASN.2018070759 10.1056/NEJMoa1208981 10.5301/jo-n.5000021 10.1111/eci.12419 10.1007/s40620-016-0288-3 10.1056/NEJMoa1615887 10.1159/000492033 10.1073/pnas.96.2.628 10.2215/CJN.06440616 |
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Keywords | Atypical hemolytic uremic syndrome eculizumab thrombotic microangiopathy protein-losing enteropathy hypoalbuminemia hemolysis |
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SubjectTerms | Atypical Hemolytic Uremic Syndrome - etiology Atypical Hemolytic Uremic Syndrome - pathology Case Report and Case Series Complement Activation Female Humans Middle Aged Monoclonal antibodies Prognosis Protein-Losing Enteropathies - complications Proteins |
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Title | Atypical hemolytic uremic syndrome in a patient with protein-losing enteropathy |
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