A case of recurrent proliferative glomerulonephritis with monoclonal IgG deposits or <i>de novo</i> C3 glomerulonephritis after kidney transplantation
-
- Tomomi Tamura
- Department of Nephrology Tokyo Women's Medical University Tokyo Japan
-
- Kohei Unagami
- Department of Nephrology Tokyo Women's Medical University Tokyo Japan
-
- Masayoshi Okumi
- Department of Urology Tokyo Women's Medical University Tokyo Japan
-
- Yoichi Kakuta
- Department of Urology Tokyo Women's Medical University Tokyo Japan
-
- Shigeru Horita
- Division of Pathology of Kidney Center Tokyo Women's Medical University Tokyo Japan
-
- Hideki Ishida
- Department of Urology Tokyo Women's Medical University Tokyo Japan
-
- Junki Koike
- Department of Pathology Kawasaki Municipal Tama Hospital Kawasaki Japan
-
- Kazuho Honda
- Department of Anatomy, School of Medicine Showa University Tokyo Japan
-
- Kazunari Tanabe
- Department of Urology Tokyo Women's Medical University Tokyo Japan
-
- Kosaku Nitta
- Department of Nephrology Tokyo Women's Medical University Tokyo Japan
書誌事項
- 公開日
- 2018-07
- 資源種別
- journal article
- 権利情報
-
- http://onlinelibrary.wiley.com/termsAndConditions#vor
- DOI
-
- 10.1111/nep.13280
- 公開者
- Wiley
この論文をさがす
説明
<jats:title>ABSTRACT</jats:title><jats:p>Proliferative glomerulonephritis with monoclonal immunoglobulin (Ig)G deposits (PGNMID) is a rare disease with a treatment that is not well established. Several cases of recurrent PGNMID after kidney transplantation have been documented, but almost all cases reported symptoms such as elevated serum creatinine and/or urinary protein levels; subsequently, episode biopsies were performed and a diagnosis was made. This is the case of a 27‐year‐old man who underwent living‐donor kidney transplantation. The aetiology of renal failure was membranoproliferative glomerulonephritis type III, which had been diagnosed at the age of 9 years. Protocol biopsy performed on postoperative day 62 revealed isolated granular C3 deposits in the glomerular capillaries and mesangium. We reviewed the native kidney biopsy and confirmed IgG3 deposition alone, with strong glomerular staining for lambda light chains and negative staining for kappa light chains. Accordingly, we re‐diagnosed the aetiology of his renal failure as PGNMID and suspected recurrent PGNMID in the early stage; therefore, we administered plasma exchange therapy. Thereafter, protocol biopsies were performed twice, which revealed persistent isolated C3 deposition; therefore, we made a diagnosis of recurrent PGNMID or C3 glomerulonephritis. Currently, the patient has normal renal function, with negative urine findings for >1 year. Here, we present the histological findings of consecutive allograft biopsies performed in this patient.</jats:p>
収録刊行物
-
- Nephrology
-
Nephrology 23 (S2), 76-80, 2018-07
Wiley
