title: Correlation of BK Virus Neutralizing Serostatus With the Incidence of BK Viremia in Kidney Transplant Recipients.
abstract: BK virus (BKV)-associated nephropathy is the second leading cause of graft loss in kidney transplant recipients. Due to the high prevalence of persistent infection with BKV in the general population, it is possible that either the transplant recipient or donor may act as the source of virus resulting in viruria and viremia. Although several studies suggest a correlation between donor-recipient serostatus and the development of BK viremia, specific risk factors for BKV-related complications in the transplant setting remain to be established.
  
  
  
  We retrospectively determined the pretransplant BKV neutralizing serostatus of 116 donors (D)-recipient (R) pairs using infectious BKV neutralization assays with representatives from the 4 major viral serotypes. The neutralizing serostatus of donors and recipients was then correlated with the incidence of BK viremia during the first year posttransplantation.
  
  
  
  There were no significant differences in baseline demographics or transplant data among the 4 neutralizing serostatus groups, with the exception of calculated panel-reactive antibody which was lowest in the D+/R- group. Recipients of kidneys from donors with significant serum neutralizing activity (D+) had elevated risk for BK viremia, regardless of recipient serostatus (D+ versus D-: odd ratio, 5.0; 95% confidence interval, 1.9-12.7]; P = 0.0008). Furthermore, donor-recipient pairs with D+/R- neutralizing serostatus had the greatest risk for BK viremia (odds ratio, 4.9; 95% confidence interval, 1.7-14.6; P = 0.004).
  
  
  
  Donor neutralizing serostatus correlates significantly with incidence of posttransplant BK viremia. Determination of donor-recipient neutralizing serostatus may be useful in assessing the risk of BKV infection in kidney transplant recipients.
authors.affiliation: 1 Novartis Institutes for BioMedical Research, Emeryville, CA. 2 University of California, San Francisco, San Francisco, CA. 3 Roche Sequencing Bioinformatics, Pleasanton, CA. 4 Massachusetts General Hospital/Harvard Medical School, Boston, MA.
authors.forename: Johanna R
authors.initials: JR
authors.lastname: Abend
authors.forename: Marguerite
authors.initials: M
authors.lastname: Changala
authors.forename: Atul
authors.initials: A
authors.lastname: Sathe
authors.forename: Fergal
authors.initials: F
authors.lastname: Casey
authors.forename: Amy
authors.initials: A
authors.lastname: Kistler
authors.forename: Sindhu
authors.initials: S
authors.lastname: Chandran
authors.forename: Abigail
authors.initials: A
authors.lastname: Howard
authors.forename: David
authors.initials: D
authors.lastname: Wojciechowski
mesh_terms: D000328:Adult; D000368:Aged; D057134:Antibodies, Neutralizing / Q000097:blood*; D000914:Antibodies, Viral / Q000097:blood*; D001739:BK Virus / Q000276:immunology*; D015415:Biomarkers / Q000097:blood; D016009:Chi-Square Distribution; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D016867:Immunocompromised Host; D007166:Immunosuppressive Agents / Q000009:adverse effects; D015994:Incidence; D016030:Kidney Transplantation / Q000009:adverse effects*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009500:Neutralization Tests; D016017:Odds Ratio; D009894:Opportunistic Infections / Q000175:diagnosis / Q000453:epidemiology / Q000276:immunology* / Q000821:virology; D027601:Polyomavirus Infections / Q000175:diagnosis / Q000453:epidemiology / Q000276:immunology* / Q000821:virology; D012189:Retrospective Studies; D012307:Risk Factors; D012495:San Francisco / Q000453:epidemiology; D013997:Time Factors; D016896:Treatment Outcome; D014412:Tumor Virus Infections / Q000175:diagnosis / Q000453:epidemiology / Q000276:immunology* / Q000821:virology
chemical_list: D057134:Antibodies, Neutralizing; D000914:Antibodies, Viral; D015415:Biomarkers; D007166:Immunosuppressive Agents