BK Virus Nephropathy in Kidney Transplant

BK polyomavirus is a ubiquitous human virus with seroprevalence over 90% in adults, primarily acquired in childhood and establishing latency in renal tubular epithelial cells and urothelium. Reactivation occurs under immunosuppression after kidney transplantation, with hierarchical progression: viruria (in urine), then viremia (in blood), and finally tissue invasion (BK nephropathy, BKVN). BKVN risk factors include intensified immunosuppression (especially tacrolimus, mycophenolate, antithymocyte globulin), cytomegalovirus coinfection, ureteric stenting, and donor-recipient HLA mismatching.

BKVN typically manifests in the first 6-12 months post-transplant with rising serum creatinine, often subclinical until biopsy. Histologic features include intranuclear viral inclusions ('decoy cells' in urine), tubular atrophy, interstitial fibrosis, and focal lymphoplasmacytic infiltrates. Distinguishing BKVN from acute T-cell mediated rejection is critical because their treatments are opposite (reduction vs intensification of immunosuppression). SV40 immunostain confirms BK infection in tissue.

Surveillance with monthly plasma BKV quantitative PCR for the first 6-12 months and quarterly thereafter is standard. Treatment is primarily immunosuppression reduction guided by viral load: if plasma BKV exceeds 10,000 copies/mL or rising trend, reduce calcineurin inhibitor and mycophenolate. Adjunctive therapies under investigation include leflunomide, cidofovir, intravenous immunoglobulin (IVIG), fluoroquinolones, and BK-specific T cell therapy. Outcomes have improved with early surveillance and intervention but graft loss still occurs in delayed cases.