Abstract: FR-PO0924
Plasmapheresis as Rescue Therapy for Early Recurrent Lupus Nephritis After Kidney Transplantation
Session Information
- Glomerular Case Reports: Lupus, FSGS, Complement, and More
November 07, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Becker, Ashley Kate, University of Central Florida HCA Healthcare GME, Greater Orlando, Orlando, Florida, United States
- Towns, Graham, Glomerular Institute, Central Florida Kidney Specialists, Orlando, Florida, United States
- Ahmed, Fawad, Glomerular Institute, Central Florida Kidney Specialists, Orlando, Florida, United States
- Sanchez Russo, Luis F., Glomerular Institute, Central Florida Kidney Specialists, Orlando, Florida, United States
Introduction
Clinical recurrence of lupus nephritis (LN) after kidney transplantation is rare but potentially devastating, often leading to allograft failure. Recurrence within the first year despite standard immunosuppression poses a significant therapeutic challenge. We present a case of early LN recurrence presenting as rapidly progressive glomerulonephritis refractory to conventional multitarget therapy, underscoring the need for alternative treatment strategies in already immunosuppressed patients.
Case Description
A 39-year-old woman with ESKD due to LN underwent living unrelated kidney transplantation (LUKT). She was not sensitized and received rabbit antithymocyte globulin for induction and maintenance immunosuppression with extended-release tacrolimus, mycophenolate, and low-dose steroids. Five months post-transplant, she presented with AKI (creatinine 1.94 mg/dL), active urine sediment (>100 RBCs/HPF), and proteinuria (UPCR 1.79). Serologies and complement levels were initially normal. Allograft biopsy revealed diffuse proliferative LN (Class IV). Despite high-dose steroids and optimization of immunosuppression, renal function worsened (creatinine peak 3.9 mg/dL) and complements declined (C3: 47, C4: 6). Low-level CMV viremia (552 IU/mL) developed, prompting valganciclovir initiation. Due to worsening function and concern for CMV, plasmapheresis was initiated in lieu of cyclophosphamide. Renal function improved, and repeat biopsy showed marked reduction in LN activity but revealed collapsing glomerulopathy. APOL1 genotyping was negative.
Discussion
This case highlights an early, treatment-refractory LN recurrence post-transplant that responded to plasmapheresis, an underutilized option in this context. Low-level CMV may have contributed to collapsing glomerulopathy in the absence of APOL1 risk variants. Early LN recurrence requires nuanced management balancing aggressive immunosuppression and infection risk, and alternative therapies such as plasmapheresis should be considered.