Abstract: PO2449
BK Polyomavirus Nephropathy After Kidney Transplantation from HCV-Infected Donor to HCV-Uninfected Recipient
Session Information
- Transplant Complications: Infection
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 1902 Transplantation: Clinical
Authors
- Abdulameer, Faisal, The University of Tennessee Health Science Center, Memphis, Tennessee, United States
- Abu Farsak, Hisham Neyazi, The University of Tennessee Health Science Center, Memphis, Tennessee, United States
- Wall, Barry M., The University of Tennessee Health Science Center, Memphis, Tennessee, United States
- Molnar, Miklos Zsolt, The University of Tennessee Health Science Center, Memphis, Tennessee, United States
Introduction
BK polyomavirus (BKPyV) is an important cause of renal allograft dysfunction. We previously published the potential association of an increased risk of BKPyV DNAemia/nephropathy in kidney transplant recipients receiving Hepatitis C (HCV) infected donor transplantation. Here, we report severe BKPyV DNAemia/nephropathy in a recipient who received HCV infected donor transplantation, which was temporally associated with initial HCV treatment failure.
Case Description
62-year-old HCV negative African American male received a cadaveric kidney transplant from a HCV infected donor in January 2019, with immediate graft function. Laboratory results 4 weeks later indicated HCV PCR of 9,310,000 IU/mL, serum creatinine 1.62 mg/dL, and BKPyV DNAemia was negative. He received glecaprevir and pibrentasvir (March 2019) for a total of 12 wk. At completion of treatment, HCV PCR was negative. Evaluation 4 weeks later revealed HCV PCR level of 482,446 IU/mL, indicating initial treatment failure. While waiting for insurance approval for coverage of secondary direct acting antiviral (DAA) regimen, he developed acute kidney injury 6 wk after HCV viremia, with serum creatinine peaking at 3.3 mg/dL along with a rapidly rising BKPyV DNAemia to >5,000,000 copies/mL. His immunosuppressive regimen was decreased. Allograft biopsy showed BKPyV nephropathy and proliferative glomerulonephritis (GN) with monoclonal IgG deposits. He was started on cidofovir, levofloxacin and intravenous immunoglobulin, followed by a course of sofosbuvir/velpatasvir/voxilaprevir and ribavirin for a total of 12 wk, achieving SVR at 12 wk. His BKPyV DNAemia slowly responded with 1,257,789 copies/mL at 6 weeks of DAA treatment and 7,378 copies/mL at 12 wk. Serum creatinine gradually improved to 2.04 mg/dL. His 1 year protocol biopsy still showed tubulointerstitial inflammation, rare positive SV40 staining, proliferative GN with improving monoclonal IgG deposits, indicating Banff borderline acute cellular rejection. His immunosuppressive regimen was intensified and graft function has remained stable.
Discussion
Our case report with close proximity of HCV treatment failure and severe BKPyV DNAemia/nephropathy supports the previous finding that transplantation from HCV infected donor kidneys to uninfected recipients may be a risk factor of BKPyV DNAemia/nephropathy.