Published online Dec 24, 2017. doi: 10.5500/wjt.v7.i6.329
Peer-review started: January 19, 2017
First decision: February 15, 2017
Revised: November 17, 2017
Accepted: December 1, 2017
Article in press: December 4, 2017
Published online: December 24, 2017
Processing time: 338 Days and 13.3 Hours
BK virus (BKV) is a polyomavirus that is able to cause renal dysfunction in transplanted grafts via BK virus-associated nephritis (BKVAN). This condition was mis-diagnosed in the past due to clinical and histopthological similarities with acute rejection. Due to the prevalence of the virus in the population, it is an important pathogen in this context, and so it is important to understand how this virus functions and its’ relationship with the pathogenesis of BKVN. Screening for BKV often reveals viruria and/or viremia, which then manifests as BKVN, which can be asymptomatic or result in clinical features namely renal dysfunction. The pathogenesis of BKV infection is still unclear and needs to be further investigated; nevertheless there are a variety of hypotheses that indicate that there are a host of factors that play important roles. Treatments for BKVAN include a reduction in immunosuppression, the use of antiviral therapy or the combination of both treatment options.
Core tip: Prior to its recognition as a separate entity, kidney transplant infection with the polyoma virus, BK virus (BKV), and the ensuing viral nephropathy (BKVN) portended a poor prognosis. But with the advent of heightened clinical suspicion and improved diagnostics the prognosis has improved considerably. Blood and urine polymerase chain reaction testing allows invasive investigation (i.e., transplant biopsy) to be selective and appropriate. Peripheral blood assays of anti-BKV cell mediated immunity offers potential for refining risk stratification. While conventional antiviral agents have failed to show utility to date, reduction of immunosuppression currently represents the most effective and proven treatment for BKVN.