BK virus (BKV) is a circular, double-stranded DNA virus that is categorized under the polyomavirus family. Nearly 80% of the adult population worldwide have antibodies to both viruses, indicating previous infection or exposure to these viruses. Initial infection with BKV is usually acquired in childhood, mostly asymptomatic or manifesting as a mild flu-like illness. After primary infection, BKV establishes latency in the kidney and bladder of the infected individual. In the setting of immunosuppression or organ transplantation, the virus reactivates and begins to replicate, triggering renal tubular cell lysis and viruria. As the reactivation progresses, the virus multiplies and crosses into the bloodstream, causing viremia and invading the kidney graft. In patients with kidney transplants, reactivation of BKV typically reaches peak incidence at 3 months posttransplantation with BK viral replication in the kidney graft, causing BKV-associated nephropathy (BKVAN), which manifests as kidney dysfunction that may result in eventual loss of the transplanted kidney. Reactivation of BKV in the bladder can lead to hemorrhagic cystitis.

After BK reactivation, the virus is first detectable in the urine, with viremia developing several weeks later. Quantitative BKV DNA in the plasma is the most widely used and preferred test for the laboratory diagnosis of BKVAN and BKV-associated hemorrhagic cystitis, as BKV viremia has higher positive predictive value (50%-60%) than BKV viruria for the diagnosis of BKVAN. Serial monitoring of BKV DNA level in plasma is recommended to guide optimal immunosuppressant dosing regimen. In those with BKVAN, clearance of BK viremia is a sign of resolution of the nephropathy.