Abstract: FR-PO1185
Mixed Acute Rejection with Plasma Cell Infiltration Responding to Bortezomib in a Kidney Transplant Recipient
Session Information
- Transplantation: Clinical - Rejection, Biomarkers, and Pharmacology
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2002 Transplantation: Clinical
Authors
- Zafar, Mohsin, SUNY Upstate Medical University Hospital, Syracuse, New York, United States
- Naseeb, Muhammad, SUNY Upstate Medical University Hospital, Syracuse, New York, United States
- Ali, Shehzad, SUNY Upstate Medical University Hospital, Syracuse, New York, United States
Introduction
Plasma cell rich acute rejection is a rare variant of T cell mediated rejection defined by more than ten percent plasma cells. Plasma cell infiltration below this threshold may still contribute to alloimmune injury when accompanied by donor specific antibodies, C4d positivity, and microvascular inflammation. This case describes mixed acute rejection with plasma cell infiltration that responded to bortezomib therapy.
Case Description
A 53 year old man with diabetic nephropathy underwent a donation after circulatory death kidney transplant with a KDPI of 34 percent. He presented with a rise in serum creatinine to 1.85 mg per dL without proteinuria. Tacrolimus trough was 13 ng per mL. Donor specific antibodies were detected and BK virus PCR was negative. Biopsy showed T cell mediated rejection IA with interstitial inflammation score 3 and tubulitis score 2, and active antibody mediated rejection with glomerulitis score 3, peritubular capillaritis score 3, diffuse C4d positivity, and circulating donor specific antibodies. Plasma cells were present but below the threshold for plasma cell rich acute rejection. Chronic injury included approximately thirty percent interstitial fibrosis and tubular atrophy and eleven percent global glomerulosclerosis. No viral cytopathic changes were identified.
Discussion
This case demonstrates a plasma cell associated rejection phenotype that does not meet the formal criteria for plasma cell rich acute rejection but still shows significant humoral activity. Plasma cells, even below the ten percent threshold, may amplify alloimmune injury when combined with donor specific antibodies, C4d positivity, and severe microvascular inflammation. These features suggest a more aggressive biology than isolated T cell mediated or antibody mediated rejection alone. The stabilization of graft function after bortezomib therapy supports the potential role of plasma cell targeted treatment in mixed rejection with plasma cell infiltration. Early recognition of this pattern may help guide more individualized immunomodulatory strategies.
Acknowledgment
We acknowledge the clinical transplant team and pathology department for their support in the evaluation and management of this case.