Hokkaido University Collection of Scholarly and Academic Papers >
Graduate School of Medicine / Faculty of Medicine >
Peer-reviewed Journal Articles, etc >
Regional secondary focal segmental glomerulosclerosis in a transplanted kidney : resolution with treatment of a segmental renal artery stenosis
This item is licensed under:Creative Commons Attribution 2.0 Generic
Title: | Regional secondary focal segmental glomerulosclerosis in a transplanted kidney : resolution with treatment of a segmental renal artery stenosis |
Authors: | Iwami, Daiki Browse this author →KAKEN DB | Harada, Hiroshi Browse this author | Usubuchi, Hiroaki Browse this author | Hotta, Kiyohiko Browse this author | Seki, Toshimori Browse this author | Togashi, Masaki Browse this author | Fukasawa, Yuichiro Browse this author |
Keywords: | Kidney transplantation | Nephrotic syndrome | Renal artery stenosis | Secondary FSGS (focal segmental glomerulosclerosis) |
Issue Date: | 12-Jun-2012 |
Publisher: | BioMed Central |
Journal Title: | BMC nephrology |
Volume: | 13 |
Start Page: | 38 |
Publisher DOI: | 10.1186/1471-2369-13-38 |
Abstract: | Background: Conditions associated with high intraglomerular filtration pressure can cause secondary focal segmental glomerulosclerosis (FSGS). Unilateral renal artery stenosis (RAS) or its occlusion results in FSGS-like changes and the nephrotic syndrome in the contralateral kidney due to hyperfiltration. However, it has been rarely reported that stenosis of a renal arterial branch can result in FSGS-like changes in a different portion in the same kidney allograft. Case presentation: A 60-year-old male kidney recipient developed allograft dysfunction after angiotensin II receptor blockade for hypertension 4 months after transplantation. It was proven that one of two arterial branches of the graft was markedly stenotic. Graft dysfunction improved after percutaneous transluminal arterioplasty (PTA), however; the stenosis recurred and massive proteinuria developed 5 months later. Graft biopsy showed ischemic changes in the region fed by the stenotic artery branch and in contrast FSGS-like changes in the region fed by the other branch. His clinicopathological manifestation including massive proteinuria almost normalized after the repeat PTA. Conclusion: Here we report a case of secondary FSGS of a kidney allograft due to severe RAS of a branch of the same kidney, in which clinical and pathological improvement were confirmed after radiological intervention. When moderate to severe proteinuria appear, secondarily developed FSGS as well as primary (recurrent or de novo) FSGS should be taken into account in kidney transplant recipients. |
Rights: | https://creativecommons.org/licenses/by/2.0/ |
Type: | article |
URI: | http://hdl.handle.net/2115/64542 |
Appears in Collections: | 医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
|
Submitter: 岩見 大基
|