Human polyoma virus-associated interstitial nephritis in the allograft kidney

Background Asymptomatic polyoma virus infection documented by urine cytolog y or serology is well known, but the clinical course of biopsy-proven inter stitial nephritis is not well defined. Methods. Twenty-two cases were identified by histology, immunostaining, in situ hybridization, electron microscopy, or polymerase chain reaction. Results, The clinical features mimicked acute rejection (n=19), chronic rej ection with incidental diagnosis at nephrectomy (n=2), or drug toxicity (n= 1), Histology showed homogenous intranuclear inclusions. In situ hybridizat ion showed BK virus (BKV) to be the predominant species, but polymerase cha in reaction documented JC virus co-infection in one of five cases so tested . Electron microscopy in seven cases showed 20-51-nm virions. The two cases diagnosed at nephrectomy received no therapy. Initial antirejection therap y in 12 cases led to clearance of the virus in 1/12 (8%), partial therapeut ic response in 3/12 (25%), and graft loss in 8/12 (67%) cases. The last rec orded creatinine in patients with functional grafts ranged from 1.9 to 7.0 (median: 4.5) mg/dl, 0.4-45 (median: 4.0) months after initial diagnosis. T he remaining eight cases treated by reduction of immunosuppression at the o utset have been free of graft loss for 0.2-10.0 (median: 4.8) months since diagnosis, and clearance of virus has been documented in three of six (50%) cases, The serum creatinine in these patients is 1.7-6.0 (median: 2.4) mg/ dl, 0.2-10 (median: 4.8) months after diagnosis. Follow-up biopsies perform ed 1-23.5 months after diagnosis show chronic allograft nephropathy. Conclusions. Polyoma virus tubulo-interstitial nephritis-associated graft d ysfunction usually calls for judicious decrease in immunosuppression and mo nitoring for acute rejection. Development of methods to serially quantify t he viral load in individual patients could potentially improve clinical out come.