Intervirology · 2004
Human polyomavirus BK monitoring by quantitative PCR in renal transplant recipients.
СтатьяНазвание и аннотация: Перевод в очереди
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Merlino Chiara, Bergallo Massimiliano, Giacchino Franca, Daniele Roberta, Bollero Christian, Comune Luciano, Segoloni Giuseppe Paolo, Cavallo Rossana
Аннотация
OBJECTIVE: To study the relation between human polyomavirus BK (BKV) infection and the risk of developing nephropathy, we monthly investigated the BKV load in urine and serum samples from 15 renal transplant recipients during 6 months in relation with immunosuppressive treatment and renal function.
METHODS: BKV-DNA in serum samples was detected by nested PCR. BKV-DNA in urine and positive serum samples was quantified by a PCR protocol developed in our laboratory.
RESULTS: Fifty-three percent of the patients had quantifiable BKV-DNA both in urine and serum samples but there was no relation between viruria and viraemia. Seventy-five percent of the patients on FK506 therapy and 71.4% of those on CyA therapy showed activation of BKV infection. No patients developed interstitial nephritis during the study. In ten patients serum creatinine levels were <2 mg/dl for the whole study, even if 80% presented BKV viruria and/ or viraemia. On the other hand, in 4 patients serum creatinine levels reached higher values, but they were BKV viruria and/or viraemia negative during the study.
CONCLUSIONS: Our results suggest that viruria and viraemia may reflect independent BKV reactivation in different tissues. The activation of the infection does not seem to be related to the type of immunosuppressive treatment nor to impairment of renal function. To better understand the pathogenetic role of BKV infection in renal transplant recipients further investigations are needed.
METHODS: BKV-DNA in serum samples was detected by nested PCR. BKV-DNA in urine and positive serum samples was quantified by a PCR protocol developed in our laboratory.
RESULTS: Fifty-three percent of the patients had quantifiable BKV-DNA both in urine and serum samples but there was no relation between viruria and viraemia. Seventy-five percent of the patients on FK506 therapy and 71.4% of those on CyA therapy showed activation of BKV infection. No patients developed interstitial nephritis during the study. In ten patients serum creatinine levels were <2 mg/dl for the whole study, even if 80% presented BKV viruria and/ or viraemia. On the other hand, in 4 patients serum creatinine levels reached higher values, but they were BKV viruria and/or viraemia negative during the study.
CONCLUSIONS: Our results suggest that viruria and viraemia may reflect independent BKV reactivation in different tissues. The activation of the infection does not seem to be related to the type of immunosuppressive treatment nor to impairment of renal function. To better understand the pathogenetic role of BKV infection in renal transplant recipients further investigations are needed.