Polyoma virus-associated interstitial nephritis in a patient with acute myeloic leukaemia and peripheral blood stem cell transplantation.

In 1971, two human polyoma viruses, BK and JC, were isolated and named after the patients in whom they were first identified [1]. BK virus (BKV) was isolated from the urine of a kidney transplant patient and JC virus (JCV) from the brain of a patient with Hodgkin’s lymphoma and progressive multifocal leukencephalopathy. Primary infection with these DNA viruses occurs early in childhood and 70–80% of adults are seropositive. After primary infection, BKV and JCV become latent in kidney and peripheral blood. Reactivation can occur spontaneously, but happens more commonly during cellular immune deficiency syndromes. Renal failure due to BKV has been described in a child with cartilage-hair hypoplasia and Hodgkin’s lymphoma [2] and in a patient with leukaemic infiltration of the kidney and polyoma virus infection [3]. Reactivation of BKV has been associated with haemorrhagic cystitis in bone marrow transplanted patients [4]. In renal transplant recipients, reactivation of BKV is increasingly recognized as a cause of severe renal-allograft dysfunction [5]. However, tubulointerstitial nephritis due to BKV in the patient’s own kidneys remains a rare condition.