Abstract: PUB333
Atypical Culprit: BK Virus-Induced AKI in a Native Kidney
Session Information
Category: Transplantation
- 2102 Transplantation: Clinical
Authors
- Ullah, Atta, Loyola University Medical Center, Chicago, Illinois, United States
- Abdulameer, Shahad, Loyola University Medical Center, Chicago, Illinois, United States
- Schneider, Julia, Loyola University Medical Center, Chicago, Illinois, United States
Introduction
BK polyomavirus nephropathy (BKPyVN) is a well-known cause of renal allograft dysfunction but remains rare and underrecognized as a cause of acute kidney injury (AKI) in lung transplant recipients with native kidneys. In immunocompromised individuals, reactivation of BK polyomavirus (BKPyV) may lead to progressive, often subclinical renal impairment. The lack of standardized screening in lung transplant patients hinders early detection and intervention.
Case Description
A 71-year-old male with scleroderma-associated ILD underwent bilateral lung transplantation in 2017. He was maintained on tacrolimus, MMF, and prednisone. Over six years, his serum creatinine rose from 1.2 mg/dL to 2.2 mg/dL, followed by an acute increase to 3.4 mg/dL in December 2023. Initial workup suggested prerenal azotemia; however, serial BKPyV PCR revealed a viral load increase from 91,972 to 1,305,120 copies/mL. A kidney biopsy on January 24, 2024, showed tubular atrophy, interstitial fibrosis, Reactive epithelial
changes, focal dense lymphoplasmacytic peritubular infiltrate with admixture of eosinophiles. Immunohistochemical staining confirmed BKPyVN. Management included discontinuation of sirolimus and administration of IVIG due to hypogammaglobulinemia. This led to a decrease in viral load to 142,224 copies/mL, but renal function continued to deteriorate, requiring peritoneal dialysis and eventual kidney transplantation.
Discussion
BKPyV-induced AKI in lung transplant recipients is rare, typically occurring around 19.5 months post-transplant. This case was unusual due to its delayed onset six years after transplant and rapid progression to end-stage renal disease (ESRD) despite timely intervention. While reduction of immunosuppression remains the primary treatment, the benefit of adjunctive therapies such as IVIG, cidofovir, and leflunomide remains unclear and requires further research. Clinicians should be aware of BKPyV induced AKI in native kidneys, particularly when more common etiologies have been excluded.