Show simple item record

dc.contributor.authorArdalan, MR
dc.contributor.authorNasri, H
dc.contributor.authorGhabili, K
dc.contributor.authorShoja, MM
dc.date.accessioned2018-08-26T08:27:35Z
dc.date.available2018-08-26T08:27:35Z
dc.date.issued2008
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/51174
dc.description.abstractObjectives: Renal allograft dysfunction can be caused by renal vessel thrombosis, acute tubular necrosis, hyperacute or acute rejection, nephrotoxicity induced by cyclosporine or tacrolimus, thrombotic microangiopathy, or urinary tract obstruction. Materials and Methods: We describe a renal transplant recipient in whom oliguria developed during the first week after transplant, although his early renal allograft function was good. Results: A Doppler ultrasonographic study revealed a lack of perfusion in the lower pole of the allograft. A perfusion defect was noted in the lower pole that was supplied by a polar artery, which had been damaged during engraftment. Light microscopy disclosed tubular cell necrosis without evidence of vascular or humoral rejection. Conclusions: We suggest that toxic molecules such as tumor necrosis factor-alpha released from a segmental infarcted area can induce tubular cell damage and necrosis leading to renal allograft dysfunction.
dc.language.isoEnglish
dc.relation.ispartofEXPERIMENTAL AND CLINICAL TRANSPLANTATION
dc.subjectKidney
dc.subjectInfarction
dc.subjectRejection
dc.subjectTransplant
dc.subjectTubular necrosis
dc.titleAcute Tubular Necrosis After Renal Allograft Segmental Infarction: The Nephrotoxicity of Necrotic Material
dc.typeArticle
dc.citation.volume6
dc.citation.issue4
dc.citation.spage312
dc.citation.epage314
dc.citation.indexWeb of science
dc.citation.URLhttp://www.ectrx.org/detail/archive/2008/6/4/0/312/0


Files in this item

FilesSizeFormatView

There are no files associated with this item.

This item appears in the following Collection(s)

Show simple item record