Polyomaviruses are a subfamily of the Papovaviridae, which includes two strands associated with disease in humans; the BK virus is produced as BK nephritis in immunosuppressed patients and JC virus which cause progressive multifocal leukoencephalopathy. The BK virus was first isolated in 1971 in England and named after the patient for whom the first viral isolate was obtained. By age 6, 60-80% of children have antibodies against BK virus. Asymptomatic viruria with BK or JC virus occurs between 10% and 45% of renal transplant recipients and 50% of bone marrow recipients secrete virus, as demonstrated by molecular studies. H After the initial episode in childhood, the virus remains latent in many organs including the uroepitheaium. Viral reactivation occurs during intensive immunosuppression. The primary infection occurs mainly in childhood as a systematic viruria that is rarely associated with clinical manifestation. The virus remains latent until reactivation occurs with intense immunosuppression. The majority of the patients with viruria are asymptomatic; However, in approximately 2-4% of these cases, the patient develops BK nephritis, manifested by an increase in serum creatinine in association with interstitial nephritis. Another manifestation of BK nephritis is ureteral stenosis with an obstructive picture following ureteral smooth muscle proliferation or ureteric ulceratio. Diagnosis of BK nephritis is made histologically after graft dysfunction which prompts a kidney biopsy to determine the etiology of graft injury. Other adjunctive tools for diagnosis the presence of "decoy cells" in the urine. Viral cultures are rarely helpful; the BK virus grows slowly, requiring weeks to months for identification. In clinical practice clinically significant polyoma virus renal disease is diagnosed by the observation of tubular viral cytopathic changes in a renal biopsy and confirmation by ancillary methods such as immunohistochemistry, electron microscopy or PCR studies. Because tubular inflammation (tubulitis) is not uncommon in polyoma virus nephritis, the differentiation between polyoma virus infection and acute rejection may be difficult. Renal tubular and urothelial cells infected with polyoma virus desquamate in the urine in quantities proportional to the degree of tissue damage. Demonstration of infected cells ("decoy cells") by examination of urine cytology is very useful in the diagnosis and follow up of patients with polyoma virus reactivy. At the present time judicious but significant decreases in immunosuppression may decrease the progression of disease. There have been a few anecdotal reports of improvement of BK nephritis after cidofovir or leflunamide treatment; at the present time, however, there is no large study performed confirming those reports.