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Abstract: PUB653

Early BK Virus-Associated Nephropathy: A Double-Edged Sword and Unbeatable Barrier for Renal Allograft Survival

Session Information

Category: Trainee Case Report

  • 1902 Transplantation: Clinical

Authors

  • Ivaturi, Kaushik, University of California, Irvine School of Medicine, Irvine, California, United States
  • Tantisattamo, Ekamol, University of California, Irvine School of Medicine, Irvine, California, United States
Introduction

The prevalence of BK virus-associated nephropathy (BKVAN) in kidney transplant (KTx) recipients is estimated to be 1 to 10%. We report a case of young woman with the first KTx complicated by an early onset BKVAN contributing to renal allograft loss.

Case Description

A 30-year-old Hispanic woman with ESRD due to reflux nephropathy underwent a 2-A-B-DR mismatched deceased donor renal transplantation with antithymocyte globulin induction. She had an immediate renal allograft function and uneventful post-KTx. Baseline serum creatinine (SCr) was 0.8 – 1.1 mg/dL. Three months post-KTx, she developed new-onset BK viremia with a serum BK virus titer of 32,889 copies/ml. A 12-hour tacrolimus level ranged between 5.1 and 7.5 ng/mL. Even after lowering mycophenolate sodium (MPS) to 360 mg twice daily, BK titer increased to 315,000 copies/ml at 8 months post-KTx. MPS was discontinued and leflunomide was started. BK virus titers progressively increased to 2 million copies/ml by 11 months post-KTx. SCr was elevated to 2.4 mg/dL. A transplant renal biopsy revealed tubulointerstitial inflammation and diffuse SV40 immunostain positivity consistent with BKVAN without evidence of acute cellular (ACR) or antibody-mediated rejections (ABMR). Even after receiving IVIG, serum BK titers continued rapidly rising up to 15 million copies/ml at 13 months post-KTx with a worsening SCr of 3.5 mg/dL. All immunosuppressive medications were discontinued and serum BK titers decreased to 2,370 copies/ml, although renal allograft function progressively worsened. Repeat transplant renal biopsy showed evidence of ABMR and 1b ACR with moderate IFTA and negative SV-40. There was no additional escalation of immunosuppressive medication and hemodialysis was initiated at 16 months post-KTx.

Discussion

Early occurrence of highly elevated level of BK viremia causing BKVAN is very difficult to treat in kidney transplant patients. Immunosuppression post- KTx can lead to BKVAN which is common cause of allograft dysfunction contributing to renal allograft loss. Both, over-immunosuppression and de-escalation should be avoided, to mitigate the risk for BKVAN, and enhance the risk for rejection respectively. Initial over-immunosuppression led to BKVAN and subsequent de-escalation led to acute rejection and ultimately allograft loss in this patient.