BACKGOUND: BK virus has emerged as a major cause of allograft loss in kidney transplant recipients over the past decade. The presence of BK virus in urine or blood indicates reactivation of the virus not necessarily accompanied by BK virus associated nephropathy. BK virus genotypes have been described based on the DNA sequence of VP1 region, and no data have been published on BK virus genotypes in Korea. In this study, we sought to determine BK virus genotypes and clinical characteristics associated with BK virus reactivation. METHODS: We isolated BK virus DNA from urine and blood of 103 kidney transplant recipients, and amplified VP1 region using polymerase chain reaction (PCR). The PCR products were sequenced and genotypes of BK virus (I-IV) were determined based on the nucleotide sequence 1744-1812 of the VP1 region. In addition, the clinical characteristics of the patients were analyzed to determine the risk factors of BK virus reactivation. RESULTS: Of 103 patients examined, 16 and 5 patients were shown to have BK viruria and viremia, respectively. Eight viral strains were demonstrated to be genotype I, but the other 8 strains neither matched with the genotypes from I to IV, nor did they fit into any other variants identified in the Western countries. Of note, 3 of these 8 unclassified strains were shown to have the same type of mutations. With respect to the risk factors of BK virus, tacrolimus and mycophenolate mofetil when combined with tacrolimus were found to be significantly associated with BK viruria and viremia. CONCLUSION: It appears that different variants of BK virus are prevalent in Korea compared with the Western countries, and that the reactivation of BK virus is significantly associated with tacrolimus.
Allografts ; Base Sequence ; BK Virus* ; DNA ; Genotype* ; Humans ; Kidney* ; Korea ; Polymerase Chain Reaction ; Risk Factors ; Tacrolimus ; Transplantation* ; Viremia

BACKGROUND: BK virus nephropathy (BKVN) has been increasingly recognized as an important cause of renal transplant dysfunction, but no specific antiviral therapy is currently available. Furthermore, a method evaluating the degree of viral infection has not been developed yet. Recently, there have been several case reports in which BKVN was successfully treated with cidofovir injection. In the current study, we report a case with BKVN successfully treated with cidofovir injection. In addition, we assessed the usefulness of quantitative viral load monitoring using a competitive polymerase chain reaction (PCR) in the treatment of BKVN. METHODS: A renal allograft recipient with BKVN was injected with cidofovir. To monitor BK viral load in urine and plasma, we developed a competitive PCR assay and followed the patient prospectively. RESULTS: A 49 year old renal transplant recipient developed a progressive rise in serum creatinine reaching 1.9 mg/dL at 15 months post-transplantation. Subsequently, the patient was diagnosed as BKVAN by allograft biopsy. At this time, BKV DNA was detected in plasma and urine. Despite a reduction of the dose of mycophenolate mofetil, serum creatinine continued to rise, which prompted the initiation of cidofovir trial. The patient was given intravenous cidofovir. After cidofovir treatment, BK virus associated findings disappeared on repeat biopsy, and BK virus in plasma was decreased to the undetectable level. For 7 months after cidofovir treatment, her renal function remained stable. CONCLUSION: Cidofovir therapy may be effective in the treatment for BKVN. Viral load in plasma reflected well the clinical and pathological course of the BK virus infection.
Allografts ; Biopsy ; BK Virus* ; Creatinine ; DNA ; Humans ; Middle Aged ; Plasma ; Polymerase Chain Reaction ; Prospective Studies ; Transplantation ; Viral Load*