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CASE REPORT
Year : 2020  |  Volume : 20  |  Issue : 3  |  Page : 186-190

Combined membranous glomerulonephritis and plasma cell-rich acute rejection in renal transplant recipient presented as nephrotic syndrome: case report and review of literature


1 Department of Nephrology, Hamed Al-Essa Organ Transplant Center, Sabah Area; Nephrology Unit, Urology and Nephrology Center, Mansoura University, Mansoura, Egypt, Kuwait
2 Department of Nephrology, Hamed Al-Essa Organ Transplant Center, Sabah Area, Kuwait
3 Department of Pathology, Faculty of Medicine, Kuwait

Correspondence Address:
Dr. Osama Gheith
Mansoura Urology and Nephrology Center, Mansoura, 35511
Kuwait
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jesnt.jesnt_12_20

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Despite the contentious trials to improve the rates of acute rejection episodes and improve the renal allograft survival with potent immunosuppressants, the occurrence of more than 10 % of the inflammatory cells infiltrating renal allograft as mature plasma cells is uncommon and was recognized as plasma cell rich acute rejection (PCAR). Combination of PCAR with other glomerulopathies has not been reported before. Here, we report a case of late-onset PCAR associated with membranous glomerulonephritis (MGN) diagnosed at an early stage (2 years after transplantation). A 58-year-old male patient had end-stage kidney disease secondary to diabetic nephropathy and he was maintained on hemodialysis for 2 years until he underwent overseas living kidney transplantation. He presented to our center in Kuwait on the sixth day postoperatively, with stable renal function. He was maintained on steroid, cyclosporine, and mycophenolate mofetil. Two years after transplant, he developed picture of nephritic syndrome. His graft biopsy showed plasma cell-rich interstitial infiltrate associated with mild edema and focal tubulitis (PCACR) in addition to MGN. Further immunohistochemistry tests revealed both B-cell and T-cell markers (CD20 and CD3) were expressed in the lymphoplasmacytic infiltrate with predominant T lymphocytes. The possibility of multiple myeloma was ruled out. He received pulse steroid 1 g od for 3 days. His maintenance immunosuppression was intensified to tacrolimus-based regimen. Cluster differentiated lymphocyte count showed high CD-19 cells; therefore, we gave him a single dose of rituximab (375 mg/m2). Follow-up graft biopsy (1 month later) revealed MGN with complete resolution of plasma cells. His proteinuria started to improve after 4 months of management. He is enjoying stable graft function with controlled diabetes mellitus. PCAR is a treatable form of acute cellular rejection, and its combination with MGN will need special care with specific CD20 ablation therapy.


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