BK virus nephropathy diagnosis and treatment: experience at the University of Maryland Renal Transplant Program.

The first case of BK virus allograft nephropathy at the University of Maryland Renal Transplant Program was diagnosed in 1997. Since then more than 100 cases have been identified. The incidence of BKAN has increased from 1% for patients transplanted in 1997 to 5.8% for patients transplanted in 2001. BKAN is an important cause of premature kidney graft loss at the University of Maryland Transplant Program. One-third of the patients diagnosed with BKAN since 1997 have already lost graft function, and a third of the remaining patients have creatinine levels over 3 mg/dl. We could not determine that a specific immunosuppressive drug increased the incidence of BKAN. Older patients had an increased risk of developing the disease. The histological diagnosis of BKAN was made at a mean time of 14.4 months after transplantation (range 1.2-53 months). BKAN occurred in 4.3% of all patients biopsied during the period described. The diagnosis of BK allograft nephropathy was based on a combination of renal biopsy to demonstrate viral cytopathic chages, urine cytology and quantitative viral load in plasma. A threshold of >10,000 copies of BK virus per ml of plasma is proposed as an indication of BKAN. Following diagnosis of BKAN, patients on a single immunosuppressve drug (FK506, CsA, sirolimus or MMF) in addition to prednisone had less graft loss and higher viral clearance in comparison to patients on prednisone and 2 immunosuppressant drugs (FK506, CsA or sirolimus and MMF). There was no difference in the rate of acute allograft rejection among different immunosuppression reduction protocols. Three patients who lost their grafts to BKAN were retransplanted. For these patients there has not yet been evidence of recurrence of BKAN. After reduction of immunosuppression, the course of BKAN in most patients followed one of 2 pathways: 1) Clearance of the infection and disappearance of the viral cytopathic changes in biopsies and urine (20%); 2)Persistence of viral replication with continuous associated tubular damage (70%). Renal transplant patients should be routinely screened with urine cytology. The presence of decoy cells in the urine is an indication for quantitative measurement of viral load in plasma. Patients with any evidence of BK viral reactivation should be followed closely. In patients biopsied early due to persistence of BK virus-infected cells in urine, there is a higher rate of conversion from positive to negative urine cytology after reduction of immunosuppression.