Plasma Cell-Rich Acute Rejection With Monoclonal Gammopathy in a Renal Transplant Recipient

dc.contributor.authorSun, In O
dc.contributor.authorYang, Chul Woo
dc.contributor.authorChoi, Yeong Jin
dc.contributor.authorKim, Yong Soo
dc.contributor.authorPark, Cheol Whee
dc.contributor.authorPark, Gyeong Sin
dc.contributor.authorChoi, Bum Soon
dc.contributor.authorChung, Byung Ha
dc.contributor.authorHong, Yu Ah
dc.contributor.authorCho, Yul Hee
dc.date.accessioned2026-05-07T10:53:38Z
dc.date.issued2013-04
dc.description.abstractPlasma cell infiltration into a renal allograft comprises a spectrum of lesions from acute rejection to posttransplant lymphoproliferative disease. We report an unusual case of plasma cell infiltration into a renal allograft with monoclonal gammopathy. A 42-year-old woman was admitted because of graft dysfunction after noncompliance with immunosuppressive therapy for 5 months. A graft biopsy showed acute T-cell–mediated rejection and massive plasma cell infiltration. Despite initial treatment with steroids and antithymocyte globulin, there was persistence of graft dysfunction, monoclonal gammopathy, and plasma cell infiltration. Subsequent treatment with bortezomib improved graft function and caused the monoclonal gammopathy to resolve. Immunohistochemical evaluation of markers of B cells (CD20 and CD138) and the ratio of kappa-to-lambda light chain (15:1) showed that infiltrating cells were plasma cells producing kappa light chain. This suggested that plasma cell-rich acute rejection with monoclonal gammopathy in this patient might have been in an early stage of kappa light chain-producing posttransplant lymphoproliferative disease confined to the renal allograft, and that bortezomib may be effective in treating a patient with this condition.
dc.identifier.issn1304-0855
dc.identifier.urihttps://hdl.handle.net/11727/15018
dc.language.isoen
dc.publisherBaşkent Üniversitesi
dc.subjectKidney
dc.subjectAntibody
dc.subjectImmunosuppression
dc.subjectBortezomib
dc.titlePlasma Cell-Rich Acute Rejection With Monoclonal Gammopathy in a Renal Transplant Recipient
dc.typeCase Report

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