Abstract: SA-PO944

One Drug’s Promise Leads to an Unavoidable Complication

Session Information

Category: Nephrology Education

  • 1302 Fellows and Residents Case Reports

Authors

  • Kowalski, Andrew, Northwestern University, Lombard, Illinois, United States
  • Fantus, Daniel, Comprehensive Transplant Center, Northwestern University, Chicago, Illinois, United States
  • Friedewald, John J., Northwestern University, Lombard, Illinois, United States
Background

CMV is a major pathogen for immunocompromised patients, especially including solid organ transplant recipients resulting in a broad range of syndromes and inducing organ rejection. This case study examins the course of denovo CMV infection in the setting of immunosupression with belatacept.

Methods

48 yo male, with a history of CKD stage V due to IgA nephropathy who underwent a successful living related kidney transplant in 7/2015. Due to his HLA status he received a steroid protocol induction and then transitioned to mycophenolate mofetil and tacrolimus. In the next few months he was transitioned to belatacept and off tacrolimus based on a study protocol.

A year later he presented with complaints of vague abdominal pain and diarrhea. He was found to have a CMV viral load of 439,804 IU/mL, and placed on ganciclovir. His viral load decreased and then rose to 55,678 IU/mL the following month despite continued ganciclovir. He complained of worsening gastrointestinal symptoms and his viral load was 152,305 IU/mL. Belatacept was stopped and tacrolimus was restarted. His creatinine was at baseline and foscarnet was started. He presented with complaints dyspnea, new onset hematuria and fevers. His creatinine was 4.45mg/dL and urine analysis had a large amount of blood and protein. Foscarnet was then held. He underwent a renal biopsy that was consistent with foscarnet induced renal toxicity.

Creatinine remained stable at 4.7mg/dL, repeated CMV viral loads were undetectable and foscarnet was discontinued. His creatinine had then peaked at 10mg/dL. His abdominal symptoms returned and his CMV viral load had increased to 41,332 IU/mL. He was readmitted for cidofovir. His creatinine had risen to 13.9mg/dL. Mycophenolate was discontinued to boost his white cell count and his CMV viral load decreased to 7000 IU/mL, but his creatinine increased to 17. He was then started on dialysis.

Conclusion

Belatacept binds to CD80 and CD86 receptors and blocks the required CD28 mediated interaction between APCs and T cells needed to activate T lymphocytes. The nature of belatacept prohibits the body to mount a response against EBV leading to an increase in PTLD. We recommend that this concern be extended to CMV negative patiens as this case shows that the use of belatacept hinders the ability of the body to mount a response leading to uncontrolled infection and nessecitating the use of nephrotoxic medications.