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Introduction: Human polyomaviruses (BK virus and JC virus) establish a latent infection in kidney (BKV) and brain (JCV) after primary infection. In case of immunosuppression, reactivation may occur causing clinical conditions. Quantitative viremia and viruria are gold standarts in diagnosing polyomavirus associated urethral stenosis and nephropathy in renal transplant recipients. In case of posttransplant nephropathy dose of the immunosupressive therapy should be increased. In polyomavirus nephropathy (PVN) on the contrary the dose of immunosupression should be reduced. The cause of nephropathy is important to adjust the dose of immunosupression in posttransplant renal transplant recipients. Materials and Methods: Two hundred seventy three plasma and urine samples of 65 renal tranplant recipients collected posttransplant at months 0, 3, 6, and 12 were investigated for quantitative polyomavirus DNA by a real-time PCR (LightCycler-LC PCR). In real-time PCR primers and probes were designed to target polyomavirus T antigen gene. BKV and JCV were identified by melting curve analysis. At pretransplant month 0, posttransplantation months 3, 6 and 12 renal biopsy specimens were investigated for BK virus infected cells by immunohistochemical methods. Results: In all of the urine samples BKV-DNA was 26.79%, 31.03%, 28.57%, and 23.53% positive, and JCV DNA was 33.93%, 51.72%, 39.29%, and 47.06% positive at months 0, 3, 6, and 12 posttransplant, respectively. When the results were compared with the healthy control group, the results of month 0 for polyomavirus DNA, JCV-DNA results of the post transplant period and BKV-DNA results of the 12 month were statistically not significant. When the results of the healthy control group and posttransplant 3 and 6 months BKV-DNA results of the renal transplant urine samples were compared we found a significant difference statistically (p= 0.014 and p= 0.025 respectively). These differences at posttransplant month 3 and 6 for BKV show a reactivation period because of intensive immunosuppression. Conclusion: In our study, BKV nephropathy was not detected in 65 renal transplant recipients with clinical, laboratory and histopathological findings. Because BKV nephropathy is found in 1-7% of renal transplant recipients a greater number of renal transplant recipients should be investigated for BKV nephropathy to find the correct incidence for our renal transplantation recipients. |
