Dendritic cell deficiency associated with development of BK viremia and nephropathy in renal transplant recipients

Karl L. Womer, Yanfei Huang, Heather Herren, Kourosh Dibadj, Ruihua Peng, Matthew Murawski, Renata Shraybman, Pamela Patton, Michael J. Clare-Salzler, Bruce Kaplan

Research output: Contribution to journalArticle

Abstract

BACKGROUND: BK virus nephropathy (BKVN) is a significant cause of renal allograft loss. Although overall intensity of immunosuppression is the greatest risk factor, recipient immune factors likely also play a role in the pathogenesis. Dendritic cells (DC) are potent antigen-presenting cells important for the induction of anti-viral cytotoxic T-cell responses. In a previous univariate analysis, we demonstrated a peripheral blood DC (PBDC) deficiency in patients with biopsy-proven BKVN, raising the possibility that reduction in DC predisposed to BK reactivation. METHODS: In this study, we refined our previous analysis by comparing random posttransplant PBDC levels between an expanded group of patients with BKVN and controls without viremia using a multivariate analysis that accounted for factors known to influence PBDC levels. Next, we compared pretransplant PBDC levels between patients stratified by the presence or absence of posttransplant viremia. Finally, we assessed the predictive value of pretransplant PBDC levels for the development of posttransplant viremia. RESULTS: Analyses revealed a PBDC level deficiency not only posttransplant in patients with BKVN but also pretransplant in patients who subsequently developed posttransplant BK viremia. Furthermore, we identified a pretransplant PBDC level that is a reasonable predictor for the development of posttransplant viremia. CONCLUSIONS: Our results identify PBDC deficiency as a previously unrecognized risk factor for BKV reactivation after renal transplantation. Pretransplant PBDC monitoring may prove to be a useful clinical tool in the assessment of patient vulnerability to BKVN posttransplant, which may allow more focused screening. copyright

Original languageEnglish (US)
Pages (from-to)115-123
Number of pages9
JournalTransplantation
Volume89
Issue number1
DOIs
StatePublished - Jan 2010

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Viremia
Dendritic Cells
BK Virus
Kidney
Transplant Recipients
Immunologic Factors
Antigen-Presenting Cells
Kidney Transplantation
Immunosuppression
Allografts
Blood Cells
Multivariate Analysis
T-Lymphocytes
Biopsy

Keywords

  • Antigen-presenting cells
  • BK virus nephropathy
  • Dendritic cells
  • Kidney transplantation.

ASJC Scopus subject areas

  • Transplantation

Cite this

Womer, K. L., Huang, Y., Herren, H., Dibadj, K., Peng, R., Murawski, M., ... Kaplan, B. (2010). Dendritic cell deficiency associated with development of BK viremia and nephropathy in renal transplant recipients. Transplantation, 89(1), 115-123. https://doi.org/10.1097/TP.0b013e3181bc6096

Dendritic cell deficiency associated with development of BK viremia and nephropathy in renal transplant recipients. / Womer, Karl L.; Huang, Yanfei; Herren, Heather; Dibadj, Kourosh; Peng, Ruihua; Murawski, Matthew; Shraybman, Renata; Patton, Pamela; Clare-Salzler, Michael J.; Kaplan, Bruce.

In: Transplantation, Vol. 89, No. 1, 01.2010, p. 115-123.

Research output: Contribution to journalArticle

Womer, KL, Huang, Y, Herren, H, Dibadj, K, Peng, R, Murawski, M, Shraybman, R, Patton, P, Clare-Salzler, MJ & Kaplan, B 2010, 'Dendritic cell deficiency associated with development of BK viremia and nephropathy in renal transplant recipients', Transplantation, vol. 89, no. 1, pp. 115-123. https://doi.org/10.1097/TP.0b013e3181bc6096
Womer, Karl L. ; Huang, Yanfei ; Herren, Heather ; Dibadj, Kourosh ; Peng, Ruihua ; Murawski, Matthew ; Shraybman, Renata ; Patton, Pamela ; Clare-Salzler, Michael J. ; Kaplan, Bruce. / Dendritic cell deficiency associated with development of BK viremia and nephropathy in renal transplant recipients. In: Transplantation. 2010 ; Vol. 89, No. 1. pp. 115-123.
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abstract = "BACKGROUND: BK virus nephropathy (BKVN) is a significant cause of renal allograft loss. Although overall intensity of immunosuppression is the greatest risk factor, recipient immune factors likely also play a role in the pathogenesis. Dendritic cells (DC) are potent antigen-presenting cells important for the induction of anti-viral cytotoxic T-cell responses. In a previous univariate analysis, we demonstrated a peripheral blood DC (PBDC) deficiency in patients with biopsy-proven BKVN, raising the possibility that reduction in DC predisposed to BK reactivation. METHODS: In this study, we refined our previous analysis by comparing random posttransplant PBDC levels between an expanded group of patients with BKVN and controls without viremia using a multivariate analysis that accounted for factors known to influence PBDC levels. Next, we compared pretransplant PBDC levels between patients stratified by the presence or absence of posttransplant viremia. Finally, we assessed the predictive value of pretransplant PBDC levels for the development of posttransplant viremia. RESULTS: Analyses revealed a PBDC level deficiency not only posttransplant in patients with BKVN but also pretransplant in patients who subsequently developed posttransplant BK viremia. Furthermore, we identified a pretransplant PBDC level that is a reasonable predictor for the development of posttransplant viremia. CONCLUSIONS: Our results identify PBDC deficiency as a previously unrecognized risk factor for BKV reactivation after renal transplantation. Pretransplant PBDC monitoring may prove to be a useful clinical tool in the assessment of patient vulnerability to BKVN posttransplant, which may allow more focused screening. copyright",
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AU - Peng, Ruihua

AU - Murawski, Matthew

AU - Shraybman, Renata

AU - Patton, Pamela

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N2 - BACKGROUND: BK virus nephropathy (BKVN) is a significant cause of renal allograft loss. Although overall intensity of immunosuppression is the greatest risk factor, recipient immune factors likely also play a role in the pathogenesis. Dendritic cells (DC) are potent antigen-presenting cells important for the induction of anti-viral cytotoxic T-cell responses. In a previous univariate analysis, we demonstrated a peripheral blood DC (PBDC) deficiency in patients with biopsy-proven BKVN, raising the possibility that reduction in DC predisposed to BK reactivation. METHODS: In this study, we refined our previous analysis by comparing random posttransplant PBDC levels between an expanded group of patients with BKVN and controls without viremia using a multivariate analysis that accounted for factors known to influence PBDC levels. Next, we compared pretransplant PBDC levels between patients stratified by the presence or absence of posttransplant viremia. Finally, we assessed the predictive value of pretransplant PBDC levels for the development of posttransplant viremia. RESULTS: Analyses revealed a PBDC level deficiency not only posttransplant in patients with BKVN but also pretransplant in patients who subsequently developed posttransplant BK viremia. Furthermore, we identified a pretransplant PBDC level that is a reasonable predictor for the development of posttransplant viremia. CONCLUSIONS: Our results identify PBDC deficiency as a previously unrecognized risk factor for BKV reactivation after renal transplantation. Pretransplant PBDC monitoring may prove to be a useful clinical tool in the assessment of patient vulnerability to BKVN posttransplant, which may allow more focused screening. copyright

AB - BACKGROUND: BK virus nephropathy (BKVN) is a significant cause of renal allograft loss. Although overall intensity of immunosuppression is the greatest risk factor, recipient immune factors likely also play a role in the pathogenesis. Dendritic cells (DC) are potent antigen-presenting cells important for the induction of anti-viral cytotoxic T-cell responses. In a previous univariate analysis, we demonstrated a peripheral blood DC (PBDC) deficiency in patients with biopsy-proven BKVN, raising the possibility that reduction in DC predisposed to BK reactivation. METHODS: In this study, we refined our previous analysis by comparing random posttransplant PBDC levels between an expanded group of patients with BKVN and controls without viremia using a multivariate analysis that accounted for factors known to influence PBDC levels. Next, we compared pretransplant PBDC levels between patients stratified by the presence or absence of posttransplant viremia. Finally, we assessed the predictive value of pretransplant PBDC levels for the development of posttransplant viremia. RESULTS: Analyses revealed a PBDC level deficiency not only posttransplant in patients with BKVN but also pretransplant in patients who subsequently developed posttransplant BK viremia. Furthermore, we identified a pretransplant PBDC level that is a reasonable predictor for the development of posttransplant viremia. CONCLUSIONS: Our results identify PBDC deficiency as a previously unrecognized risk factor for BKV reactivation after renal transplantation. Pretransplant PBDC monitoring may prove to be a useful clinical tool in the assessment of patient vulnerability to BKVN posttransplant, which may allow more focused screening. copyright

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