BK Polyomavirus in Solid Organ Transplantation

TLDR

BK polyomavirus is the leading cause of polyomavirus‑associated nephropathy, threatening graft survival in 1–15 % of kidney transplant recipients, and late diagnosis leads to irreversible decline while evidence for adjunct therapies remains unproven. The study seeks to determine whether screening kidney transplant recipients for BKV replication can guide immunosuppression reduction. This is accomplished by testing urine and blood for BKV to identify viremia and inform treatment decisions. Screening and subsequent immunosuppression reduction expands BKV‑specific cellular immunity, curtails graft replication, and clears viremia in 70–90 % of patients, with post‑intervention rejection occurring in 8–12 % (mostly steroid responsive) and retransplantation after PyVAN being largely successful when closely monitored for recurrence.

Abstract

The human BK polyomavirus (BKV) is the major cause of polyomavirus-associated nephropathy (PyVAN) putting 1-15% of kidney transplant patients at risk of premature allograft failure, but is less common in other solid organ transplants. Because effective antiviral therapies are lacking, screening kidney transplant patients for BKV replication in urine and blood has become the key recommendation to guide the reduction of immunosuppression in patients with BKV viremia. This intervention allows for expanding BKV-specific cellular immune responses, curtailing of BKV replication in the graft, and clearance of BKV viremia in 70-90% patients. Postintervention rejection episodes occur in 8-12%, most of which are corticosteroid responsive. Late diagnosis is faced with irreversible functional decline, poor treatment response, and graft loss. Adjunct therapies such as cidofovir, leflunomide and intravenous immunoglobulins have been used, but the benefit is not documented in trials. Retransplantation after PyVAN is largely successful, but requires close monitoring for recurrent BKV viremia.