AbstractPurpose of review
Increasing prevalence of BK virus nephritis after renal transplantation has prompted review of important publications on this topic.Recent findings
Nephritis from the BK virus occurs specifically in renal transplant recipients, but not after other solid organ transplantation. A mouse renal transplant model of polyoma nephritis unveils the role of alloimmune activity in the development of BK virus nephritis. BK virus nephritis occurs approximately 1 year after transplantation, as opposed to acute rejection, which occurs early after transplantation. No identifiable donor, recipient, or transplant variables correlate with this disease. Recipients who receive a kidney from a seropositive kidney donor and the lack of HLA C7 in either donor or recipient may play a role in BK virus infection. Mycophenolate mofetil and tacrolimus combination therapy is associated with a slightly higher chance of infection. Recovery from BK virus nephritis is associated with increase in BK virus-specific humoral and cellular immunity, which suggests that they are relevant factors in the pathogenesis of this disease.Summary
Nephritis from BK virus infection occurs through seropositive donors. Lack of HLA C7 in donor and recipient and BK virus-specific humoral and cellular immune deficiencies may precipitate infection.