Introduction Clinical Setting

The BK polyoma virus virus was originally isolated from B.K., a Sudanese patient who had distal donor ureteral stenosis months after a living related transplant (9). BK virus is related to JC virus (which also inhabits the human urinary tract) and to simian kidney virus SV-40. These viruses are members of the papovavirus group, which includes the papilloma viruses. The BK virus commonly infects urothelium but rarely causes morbidity in immunocompetent individuals. However, in renal transplant recipients three lesions have been attributed to BK virus: hemorrhagic cystitis, ureteral stenosis, and acute interstitial nephritis (10,11). In a prospective study of 48 renal transplant recipients, active polyomavirus (BK or JC) infection was shown in 65%; 68% of these had intranuclear inclusions in urine cytology (12). Half of infections occurred within the first 3 months after transplantation, but some occurred 2 years or longer afterward. In 26% renal function became impaired at the time of the polyomavirus infection but no biopsy was done. A seropositive donor increased the rate of primary or reactivation infections with BK virus (13).

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