BK transplant nephropathy successfully treated with cidofovir

BK‐virus‐induced interstitial nephritis (BK nephropathy) is a recently recognized condition affecting renal allografts that may lead to graft failure [1]. BK‐virus infection is endemic worldwide with seroprevalence rates in normal adults of 60–80% [1]. Risk factors for BK nephropathy include high levels of immunosuppression, particularly involving tacrolimus [2]. There is no established treatment other than reduction of immunosuppression to aid viral clearance, which risks acute irreversible rejection [3]. There are in vitro data showing that cidofovir inhibits BK virus replication, but there are no studies in renal transplant recipients [4]. We report a case of BK nephropathy successfully treated with intravenous cidofovir and a modest reduction in immunosuppression. A 47‐year‐old male with chronic renal failure due to an undefined chronic glomerulonephritis received a non‐HLA matched kidney transplant from his wife in July 2001. BK virus was undetectable by polymerase chain reaction (PCR) in the donor's blood and urine following the transplant. The recipient's comorbidities included hypertension, hypercholesterolaemia, gastro‐oesophageal reflux and gout. The initial immunosuppression used was prednisolone, sirolimus and tacrolimus as part of a clinical trial. There were no episodes of clinical rejection in the first 6 months post‐transplantation. A biopsy performed at insertion and day 10 showed no evidence of rejection or BK viral infection. The only significant early complication was the development of type 2 diabetes mellitus. At 6 months his baseline serum creatinine level was 0.13 mmol/l (0.05–0.12 mmol/l).