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dc.contributor.authorMatos, Ana Cristina
dc.contributor.authorCâmara, Niels Olsen Saraiva [UNIFESP]
dc.contributor.authorRequiao-Moura, Lucio R.
dc.contributor.authorTonato, Eduardo J.
dc.contributor.authorFiliponi, Thiago C.
dc.contributor.authorSouza-Durao, Marcelino, Jr.
dc.contributor.authorMalheiros, Denise M.
dc.contributor.authorFregonesi, Mauricio
dc.contributor.authorBorrelli, Milton
dc.contributor.authorPacheco-Silva, Alvaro [UNIFESP]
dc.date.accessioned2020-07-31T12:47:27Z
dc.date.available2020-07-31T12:47:27Z
dc.date.issued2016
dc.identifierhttp://dx.doi.org/10.1111/nep.12699
dc.identifier.citationNephrology. Hoboken, v. 21, n. 11, p. 923-929, 2016.
dc.identifier.issn1320-5358
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/56841
dc.description.abstractAim: The role of post-reperfusion biopsy findings as a predictor of early and long-term graft function and survival is still a target of research. Methods: We analyzed data from 136 post-reperfusion biopsies performed in deceased donor renal transplanted patients from November 2008 to May 2012. We analyzed the presence of acute tubular necrosis (ATN), arteriolar hyalinosis (AH), intimal thickness (IT), interstitial fibrosis (IF) and glomerulosclerosis (GS). We also analyzed the impact of donor features on the following outcomes: delayed graft function (DGF) and chronic allograft dysfunction defined as eGFR < 60mL/min at 1 year. Results: The mean donor age was 41 years, 26% of whom were extended criteria donors (ECD), 33% had hypertension and 50% had cerebral vascular accident (CVA) as the cause of death. ATN was present in 87% of these biopsies, AH in 31%, IF in 21%, IT in 27% and GS in 32%. DGF occurred in 80% and chronic allograft dysfunction was present in 53%. AHwas the only histological finding associated with DGF and chronic allograft dysfunction at 1 year. Patients with AH had a lower eGFR at 1 year than patients without it (49.8 mL/min x 64.5 mL/min, P= 0.02). In the multivariate analysis, risk variables for development of chronic graft dysfunction were male sex (odds ratio [OR] = 3.159 [CI: 1.22-8.16]en
dc.description.abstractP= 0.018), acute rejection (OR = 8.91 [CI: 2.21-35.92]en
dc.description.abstractP= 0.002), donor hypertension (OR = 2.94 [CI: 1.10-7.84]en
dc.description.abstractP= 0.031), AH (OR = 3.96 [CI: 1.46-10.70]en
dc.description.abstractP= 0.007) and eGFR at discharge (OR = 0.96 [CI: 0.93-0.98]en
dc.description.abstractP= 0.005). In multivariate analysis, risk factors for AH were donor age >= 50 years (OR =2.46 [CI: 1.10-5.44]en
dc.description.abstractP=0.027) and CVA as the cause of donor death (OR =2.33 [CI: 1.05-5.15]en
dc.description.abstractP=0.007). Conclusion: The presence of AH in post-reperfusion biopsies is a marker of ageing and vascular disease and was associated with DGF and a one year poorer renal function. AH in donor biopsies superimposed to long ischaemic time is a predictor of renal function. The management of immunosuppression based on the presence of AH in post-reperfusion biopsy could be useful to improve long term graft function.en
dc.format.extent923-929
dc.language.isoeng
dc.publisherWiley-Blackwell
dc.relation.ispartofNephrology
dc.rightsAcesso restrito
dc.subjectchronic allograft nephropathyen
dc.subjectglomerular filtration rateen
dc.subjectischaemia-reperfusionen
dc.subjectpathologyen
dc.subjectrenalen
dc.subjectrenal biopsyen
dc.subjecttransplantationen
dc.titlePresence of arteriolar hyalinosis in post-reperfusion biopsies represents an additional risk to ischaemic injury in renal transplanten
dc.typeArtigo
dc.description.affiliationHosp Israelita Albert Einstein, Renal Transplant Div, Ave Albert Einstein 627-701, Sao Paulo, SP, Brazil
dc.description.affiliationUniv Fed Sao Paulo, Nephrol Dept, Sao Paulo, Brazil
dc.description.affiliationUniv Sao Paulo, Immunol Dept, Sao Paulo, Brazil
dc.description.affiliationHosp Israelita Albert Einstein, Pathol Dept, Sao Paulo, Brazil
dc.description.affiliationUnifespNephrology Department, Universidade Federal de São Paulo (UNIFESP), São Paulo, Brazil
dc.identifier.doi10.1111/nep.12699
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000385715400003
dc.coverageHoboken
dc.citation.volume21
dc.citation.issue11


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