Abstract: SA-PO1137
Control of Refractory Resistant Cytomegalovirus Viremia After Belatacept Withdrawal in a High-Risk Kidney Transplant Recipient
Session Information
- Transplantation: Clinical - Infectious Diseases
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2002 Transplantation: Clinical
Authors
- Maturostrakul, Boonyanuth N., Baystate Medical Center, Springfield, Massachusetts, United States
- Agarwal, Krishna A., Baystate Medical Center, Springfield, Massachusetts, United States
- DelPilar Morales, Esteban A., Baystate Medical Center, Springfield, Massachusetts, United States
- Saha, Urmee, Baystate Medical Center, Springfield, Massachusetts, United States
- Paez, Armando, Baystate Medical Center, Springfield, Massachusetts, United States
Introduction
Belatacept is used to avoid calcineurin inhibitor toxicity after kidney transplantation but has been associated with increased incidence and severity of cytomegalovirus (CMV) infection, particularly in CMV donor-positive/recipient-negative (D+/R–) recipients.
Case Description
A 52-year-old man with ESRD from ANCA vasculitis and anti-GBM disease underwent deceased-donor kidney transplantation with thymoglobulin induction. Donor was CMV seropositive and recipient seronegative. Prolonged delayed graft function prompted early conversion from tacrolimus to belatacept. Maintenance immunosuppression consisted of belatacept, mycophenolate sodium, and prednisone.
Four months post-transplant, he developed CMV viremia. Valganciclovir was escalated to treatment dosing and mycophenolate was held, with transient viral suppression followed by recurrent viremia. Therapy was transitioned to maribavir. Resistance testing demonstrated ganciclovir and cidofovir resistance and preserved susceptibility to maribavir, foscarnet, and letermovir.
Despite maribavir, CMV viral load rose progressively, peaking at 65,039 IU/mL, 9 months following Belatacept conversion. Foscarnet was avoided due to concern for nephrotoxicity. Belatacept was discontinued, and transitioned to sirolimus with prednisone. Following belatacept withdrawal, CMV viral load declined and remained <200 IU/mL, at 6 weeks from last Belatacept dose. Subsequent repeat CMV resistance testing 2 months after prior test found maribavir resistance,prompted transition to letermovir as prohylaxis. The patient remained asymptomatic without tissue-invasive disease, and serum creatinine remained stable ~2.3 mg/dL.
Discussion
Belatacept increases the risk of severe and prolonged CMV infection in CMV D+/R– recipients, by blocking the CD28-CD80/86 costimulatory pathway crucial for naive T cell activation. This case highlights refractory CMV viremia with sequential antiviral resistance in a CMV D+/R– kidney transplant recipient receiving belatacept-based immunosuppression. Despite active antiviral therapy, virologic control was not achieved until belatacept discontinuation, suggesting that impaired CMV-specific cellular immunity may have contributed substantially to persistent infection. This case highlights the need to reassess immunosuppression alongside antiviral therapy in refractory CMV infection.