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Publicação:
Histopathological features of thrombotic microangiopathies in renal biopsies

dc.contributor.authorNeto, Miguel Ernandes [UNESP]
dc.contributor.authorSoler, Lucas de Moraes [UNESP]
dc.contributor.authorVasconcelos, Halita Vieira Gallindo [UNESP]
dc.contributor.authorDos Santos, Daniela Cristina [UNESP]
dc.contributor.authorViero, Rosa Marlene [UNESP]
dc.contributor.authorde Andrade, Luís Gustavo Modelli [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.contributor.institutionHospital BP – a Beneficência Portuguesa de São Paulo
dc.date.accessioned2022-05-01T09:30:33Z
dc.date.available2022-05-01T09:30:33Z
dc.date.issued2019-01-01
dc.description.abstractBackground: Thrombotic microangiopathy (TMA) is a morphologic lesion characterized by thrombi occluding microvasculature related to endothelial injury. Objectives: This study aimed to assess the association between histopathological findings and etiology of TMA. Patients and Methods: This cross-sectional study comprised a sample of 34 patients who underwent renal biopsy and received an initial TMA diagnoses resulting in 29 definitive TMA cases. We evaluated the TMA features and clinical histopathological correlation. Results: The most frequent etiologies were atypical hemolytic uremic syndrome (aHUS) (n= 10; 34.5%), hemolytic uremic syndrome caused by Shiga toxin-producing Escherichia coli (STEC-HUS) (n=6; 24.1%) and secondary causes of TMA (n= 12; 41.4%). We found the following histological features; patients with aHUS had thrombi in 60% of biopsies, membranoproliferative glomerulonephritis (MPGN)-like pattern in 20% and ischemia in 20%; patients with STEC-HUS had thrombi (14.3%), MPGN-like pattern (14.3%), endothelial swelling (14.3%) and ischemia (57.1%); patients with secondary etiologies had thrombi (58.3%), endothelial swelling (16.7%), ischemia (16.7%) and MPGN-like pattern (8.3%). Conclusions: The distribution of classic TMA findings was not related to etiology in spite of micro-thrombi having been found mostly in aHUS and secondary etiologies, whereas ischemia was found mainly in STEC-HUS. We did not find a histopathological pattern to each etiology of TMA.en
dc.description.affiliationDepartment of Internal Medicine São Paulo State University (UNESP)
dc.description.affiliationHospital BP – a Beneficência Portuguesa de São Paulo
dc.description.affiliationDepartment of Pathology São Paulo State University (UNESP)
dc.description.affiliationUnespDepartment of Internal Medicine São Paulo State University (UNESP)
dc.description.affiliationUnespDepartment of Pathology São Paulo State University (UNESP)
dc.identifierhttp://dx.doi.org/10.15171/JNP.2019.27
dc.identifier.citationJournal of Nephropathology, v. 8, n. 3, 2019.
dc.identifier.doi10.15171/JNP.2019.27
dc.identifier.issn2251-8819
dc.identifier.issn2251-8363
dc.identifier.scopus2-s2.0-85115204488
dc.identifier.urihttp://hdl.handle.net/11449/233554
dc.language.isoeng
dc.relation.ispartofJournal of Nephropathology
dc.sourceScopus
dc.subjectEndothelium
dc.subjectHemolytic uremic syndrome
dc.subjectMicrothrombi
dc.subjectShiga toxin
dc.subjectThrombotic microangiopathy
dc.titleHistopathological features of thrombotic microangiopathies in renal biopsiesen
dc.typeArtigo
dspace.entity.typePublication
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Medicina, Botucatupt
unesp.departmentPatologia - FMBpt

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