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Abstract: SA-PO047

Native BK Polyomavirus Nephropathy in an Orthotopic Heart Transplant Recipient

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical‚ Outcomes‚ and Trials


  • Thompson, Zachary M., Baylor College of Medicine, Houston, Texas, United States
  • Ajene, George O., Baylor College of Medicine, Houston, Texas, United States
  • Kandary, Mark, Baylor College of Medicine, Houston, Texas, United States
  • Kulkarni, Prathit A., Baylor College of Medicine, Houston, Texas, United States
  • Aggarwal, Nidhi, Baylor College of Medicine, Houston, Texas, United States
  • Fedson, Savitri, Baylor College of Medicine, Houston, Texas, United States
  • Shah, Maulin, Baylor College of Medicine, Houston, Texas, United States

BK polyomavirus nephropathy (BKVN) is a common cause of kidney allograft dysfunction. It typically occurs within the first year post-transplantation. BKVN in native kidneys after extra-renal solid-organ transplantation (SOT) is unusual. Here, we report a case of native BKVN occurring 13 years after orthotopic heart transplant (OHT).

Case Description

A 75-year-old man with Grade 3b chronic kidney disease presented with acute kidney injury. He had undergone OHT 13 years prior with stable allograft function and no recent episodes of rejection. His immunosuppressive regimen consisted of tacrolimus, sirolimus, and mycophenolate mofetil (MMF). Three months prior to presentation, he had developed obstructive ureterolithiasis requiring ureteral stenting. Imaging at the time of his current presentation showed resolution of prior ureteral obstruction. Serum levels of immunosuppressive agents were within therapeutic range. The serum BK viral load was 362,000 copies/ml. Kidney biopsy revealed acute tubular injury with focal viral cytopathic changes and SV40 staining within tubular epithelium, consistent with BKVN. Immunosuppression was reduced by stopping sirolimus and exchanging MMF for leflunomide with subsequent improvement in kidney function.


While BK virus seropositivity is common worldwide, BKVN is almost exclusively seen in kidney transplant patients. Native-kidney BKVN after extra-renal SOT is uncommon. Intensity of immunosuppression is a well-known risk factor for viral replication; ureteral stenting has also been associated with BKVN. However, since clinical manifestations of BKV infection often include genitourinary (GU) tract pathology, ureteral strictures may be either a symptom or risk factor of infection. Although rare, it is important for clinicians consider BKVN even in patients with non-renal SOT, especially in the clinical context of known GU disease.

Treatment of native BKVN is based on experience from treatment of BKVN in kidney transplant patients. While there are no randomized controlled trials, the current mainstay of treatment is reduction of immunosuppression, backed by meta-analyses and observational studies. Additional possible therapies without strong evidence include intravenous immunoglobulin, leflunomide, cidofovir, brincidofovir, and fluoroquinolones.