Ilkka Helanterä1, Hans H Hirsch2, Eeva Auvinen3, Laura Mannonen3, Maaret Nummi3, Marion Wernli4, Fernanda Ortiz5, Anne Räisänen-Sokolowski6, Marko Lempinen7, Irmeli Lautenschlager3. 1. Transplantation and Liver Surgery, University of Helsinki and Helsinki University Hospital, PO Box 372, FI 00029 HUS, Helsinki, Finland. Electronic address: Ilkka.helantera@helsinki.fi. 2. Transplantation and Clinical Virology, Department of Biomedicine, University of Basel, Petersplatz 10, CH-4009 Basel, Switzerland; Infectious Diseases & Hospital Epidemiology, University Hospital Basel, Petersgraben 4, CH-4031 Basel, Switzerland. 3. Department of Virology, University of Helsinki and Helsinki University Hospital (HUSLAB), PO Box 400, FI 00029 HUS, Helsinki, Finland. 4. Transplantation and Clinical Virology, Department of Biomedicine, University of Basel, Petersplatz 10, CH-4009 Basel, Switzerland. 5. Department of Nephrology, University of Helsinki and Helsinki University Hospital, PO Box 372, FI 00029 HUS, Helsinki, Finland. 6. Department of Pathology, University of Helsinki and Helsinki University Hospital (HUSLAB), PO Box 400, FI 00029 HUS, Helsinki, Finland. 7. Transplantation and Liver Surgery, University of Helsinki and Helsinki University Hospital, PO Box 372, FI 00029 HUS, Helsinki, Finland.
Abstract
BACKGROUND: The significance of JC polyomavirus (JCPyV) after kidney transplantation ranges from irrelevant to full-blown nephropathy or PML. OBJECTIVES: To investigate the clinical significance of high-level JCPyV viruria and JCPyV primary infections after kidney transplantation. STUDY DESIGN: JCPyV viruria was detected in routine screening by quantitative real-time PCR in 40/238 kidney transplant recipients and was high-level (>107 copies/ml) in 17 patients. A protocol biopsy at the time of JCPyV viruria was available from 10 patients. RESULTS: Peak urine viral loads were 1.0×107-2.5×109 copies/ml in the 17 high-level viruria patients. 6/15 (40%) patients with high-level JCPyV viruria with pretransplant sera available were JCPyV IgG negative suggesting that JCPyV viruria resulted from the donor graft in most cases. No acute graft dysfunction was associated with JCPyV viruria. No positive SV40 staining was detected in protocol biopsies, and no specific histopathology was associated with high-level viruria; JCPyV nephropathy was not found. No differences were seen in histopathology or graft function at 3 years in patients with high-level viruria compared to non-JCPyV viruric patients transplanted during the same time period, and outcome was similar in patients with presumably primary and reactivated JCPyV. The mean estimated GFR at last follow-up was 44ml/min (range 12-60ml/min). One graft with high-level viruria was lost 9 years posttransplant due to recurrent IgA nephropathy CONCLUSIONS: High-level JCPyV viruria seems to be associated with primary JCPyV infection reflecting the average seroprevalence of 60%, but is not stringently associated with inferior graft function or survival, or histopathological changes. Copyright Â
BACKGROUND: The significance of JC polyomavirus (JCPyV) after kidney transplantation ranges from irrelevant to full-blown nephropathy or PML. OBJECTIVES: To investigate the clinical significance of high-level JCPyV viruria and JCPyVprimary infections after kidney transplantation. STUDY DESIGN:JCPyV viruria was detected in routine screening by quantitative real-time PCR in 40/238 kidney transplant recipients and was high-level (>107 copies/ml) in 17 patients. A protocol biopsy at the time of JCPyV viruria was available from 10 patients. RESULTS: Peak urine viral loads were 1.0×107-2.5×109 copies/ml in the 17 high-level viruria patients. 6/15 (40%) patients with high-level JCPyV viruria with pretransplant sera available were JCPyV IgG negative suggesting that JCPyV viruria resulted from the donor graft in most cases. No acute graft dysfunction was associated with JCPyV viruria. No positive SV40 staining was detected in protocol biopsies, and no specific histopathology was associated with high-level viruria; JCPyVnephropathy was not found. No differences were seen in histopathology or graft function at 3 years in patients with high-level viruria compared to non-JCPyV viruric patients transplanted during the same time period, and outcome was similar in patients with presumably primary and reactivated JCPyV. The mean estimated GFR at last follow-up was 44ml/min (range 12-60ml/min). One graft with high-level viruria was lost 9 years posttransplant due to recurrent IgA nephropathy CONCLUSIONS: High-level JCPyV viruria seems to be associated with primary JCPyV infection reflecting the average seroprevalence of 60%, but is not stringently associated with inferior graft function or survival, or histopathological changes. Copyright Â
Authors: Britta Höcker; Julia Tabatabai; Lukas Schneble; Jun Oh; Florian Thiel; Lars Pape; Krisztina Rusai; Rezan Topaloglu; Birgitta Kranz; Günter Klaus; Nikoleta Printza; Onder Yavascan; Alexander Fichtner; Kai Krupka; Thomas Bruckner; Rüdiger Waldherr; Michael Pawlita; Paul Schnitzler; Hans H Hirsch; Burkhard Tönshoff Journal: Pediatr Nephrol Date: 2018-07-30 Impact factor: 3.714
Authors: Peter W Schreiber; Verena Kufner; Kerstin Hübel; Stefan Schmutz; Osvaldo Zagordi; Amandeep Kaur; Cornelia Bayard; Michael Greiner; Andrea Zbinden; Riccarda Capaul; Jürg Böni; Hans H Hirsch; Thomas F Mueller; Nicolas J Mueller; Alexandra Trkola; Michael Huber Journal: Clin Infect Dis Date: 2019-08-30 Impact factor: 9.079