Abstract: TH-PO0928
Low-Level BK Virus Can Trigger Systemic Thrombotic Microangiopathy in a Kidney Transplant Recipient
Session Information
- Transplantation: Clinical - Glomerular Diseases, Infections, and Rejection
November 06, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2102 Transplantation: Clinical
Authors
- Naseeb, Muhammad, SUNY Upstate Medical University Hospital, Syracuse, New York, United States
- Ali, Shehzad, SUNY Upstate Medical University Hospital, Syracuse, New York, United States
- Aslam, Muhammad Haseeb, SUNY Upstate Medical University Hospital, Syracuse, New York, United States
- Min, Brian, SUNY Upstate Medical University Hospital, Syracuse, New York, United States
- Shafqat, Mahzaib, Allama Iqbal Medical College, Lahore, Punjab, Pakistan
- Budhathoki, Sabita, SUNY Upstate Medical University Hospital, Syracuse, New York, United States
- Amit, Alimul Bari, SUNY Upstate Medical University Hospital, Syracuse, New York, United States
- Mahboob, Muhammad Junaid, SUNY Upstate Medical University Hospital, Syracuse, New York, United States
- Rehman, Tanzeel, SUNY Upstate Medical University Hospital, Syracuse, New York, United States
Group or Team Name
- Upstate Nephrology Department, Upstate Medical University Hospital.
Introduction
Thrombotic microangiopathy (TMA) is a rare but severe complication in kidney transplant recipients, often linked to calcineurin inhibitors, antibody-mediated rejection, or genetic predisposition. However, viral infections like CMV, Parvovirus are attributed to it, but not usually the BK virus. Here we present a low BK virus as a trigger for systemic TMA.
Case Description
53 y.o. female s/p preemptive deceased donor kidney transplant with KDPI 15% on 5/2/2016 with immediate graft function, for the treatment of her ESRD. The patient has a high risk for rejection with a pre-transplant PRA of 84%. The recipient was treated with 6 doses of Thymoglobulin for induction and has been maintained on tacrolimus, mycophenolate, and prednisone.
In 11/24 patient was found to have elevated creatinine, and biopsy revealed cellular rejection; DSA and C4d were negative. She received treatment for cellular rejection. Repeat biopsy in 1/25 with increased creatinine and plasma cells received steroids and two doses of bortezomibe, and creatinine stabilized.
She came back 2-3 weeks after for follow-up and was noted to have increased LFTs, thrombocytopenia, and schistocytes. Thorough workup shows negative CMV, EBV, Parvo virus, and ADAMTs 13. Creatinine remained stable, but further workup for systemic TMA found to have low levels of BK virus, 58.9 IU/ml and 74.9 IU/ml.
All immunosuppression and other medications were decreased and reviewed with the patient. But in this case, low-level BK virus is a potential trigger for systemic TMA. In the next couple of months, schistocytes disappeared, platelet count normalized. She got eculizumab for 3 months. Genetic testing: still pending result to date.
Discussion
This case highlights the potential for low-level BKV replication as a trigger to systemic TMA in kidney transplant recipients. While the exact mechanism remains unclear, possible pathways include direct endothelial injury, immune activation, and complement dysregulation. This report underscores the need for regular BKV monitoring and early adjustment of immunosuppressive therapy to prevent severe complications. This case shows that even low-level BK virus can trigger a systemic TMA in a solid organ transplant patient.