The pathogenesis of acute allograft dysfunction in desensitized renal transplant recipients

Background Acute allograft rejection after HLA desensitization is common early post‐transplant but the sequence of histopathologic changes leading to graft dysfunction has not been well defined. Methods We evaluated the early pathogenesis and sequence of antibody‐mediated graft damage of 35 desensit...

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Published inClinical transplantation Vol. 26; no. 4; pp. E402 - E411
Main Authors Singh, N., Sun, Q., Nadasdy, T., Adams, P., DiPaola, N.R., Pesavento, T., Winters, H., Satoskar, A., Yu, Z., Henry, M., Hadley, G.A., Pelletier, R.P.
Format Journal Article
LanguageEnglish
Published Denmark Blackwell Publishing Ltd 01.07.2012
Subjects
antibody
desensitization
Desensitization, Immunologic
Flow Cytometry
Follow-Up Studies
Graft Rejection - immunology
Graft Rejection - pathology
HLA
HLA Antigens - immunology
Humans
Isoantibodies - blood
Isoantibodies - immunology
Kidney Transplantation - immunology
Kidney Transplantation - pathology
Prognosis
rejection
renal transplant
Retrospective Studies
Transplantation, Homologous
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Abstract Background Acute allograft rejection after HLA desensitization is common early post‐transplant but the sequence of histopathologic changes leading to graft dysfunction has not been well defined. Methods We evaluated the early pathogenesis and sequence of antibody‐mediated graft damage of 35 desensitized living donor kidney recipients by studying the course of biopsies taken in the very early post‐transplant period (<1 month). Results A total of 14 of the 35 patients met criteria for acute antibody‐mediated rejection (AMR). In these patients, the chronologic sequence of pathologic changes was C4d peritubular capillary deposition, acute tubular injury, and peritubular capillaritis, followed by glomerulitis and interstitial inflammation. Classic AMR lesions occurred early, followed by mononuclear cellular infiltration, which comprised CD4 and CD8 T cells and monocytes. Development of graft dysfunction in most patients occurred concurrently with the emergence of graft cellular infiltration, rather than at the earlier time of antibody deposition as detected via C4d deposition. Conclusion These data provide novel insight into the sequence of pathologic changes in patients with AMR post‐transplant after HLA desensitization.
AbstractList Acute allograft rejection after HLA desensitization is common early post-transplant but the sequence of histopathologic changes leading to graft dysfunction has not been well defined. We evaluated the early pathogenesis and sequence of antibody-mediated graft damage of 35 desensitized living donor kidney recipients by studying the course of biopsies taken in the very early post-transplant period (<1 month). A total of 14 of the 35 patients met criteria for acute antibody-mediated rejection (AMR). In these patients, the chronologic sequence of pathologic changes was C4d peritubular capillary deposition, acute tubular injury, and peritubular capillaritis, followed by glomerulitis and interstitial inflammation. Classic AMR lesions occurred early, followed by mononuclear cellular infiltration, which comprised CD4 and CD8 T cells and monocytes. Development of graft dysfunction in most patients occurred concurrently with the emergence of graft cellular infiltration, rather than at the earlier time of antibody deposition as detected via C4d deposition. These data provide novel insight into the sequence of pathologic changes in patients with AMR post-transplant after HLA desensitization.
BACKGROUNDAcute allograft rejection after HLA desensitization is common early post-transplant but the sequence of histopathologic changes leading to graft dysfunction has not been well defined.METHODSWe evaluated the early pathogenesis and sequence of antibody-mediated graft damage of 35 desensitized living donor kidney recipients by studying the course of biopsies taken in the very early post-transplant period (<1 month).RESULTSA total of 14 of the 35 patients met criteria for acute antibody-mediated rejection (AMR). In these patients, the chronologic sequence of pathologic changes was C4d peritubular capillary deposition, acute tubular injury, and peritubular capillaritis, followed by glomerulitis and interstitial inflammation. Classic AMR lesions occurred early, followed by mononuclear cellular infiltration, which comprised CD4 and CD8 T cells and monocytes. Development of graft dysfunction in most patients occurred concurrently with the emergence of graft cellular infiltration, rather than at the earlier time of antibody deposition as detected via C4d deposition.CONCLUSIONThese data provide novel insight into the sequence of pathologic changes in patients with AMR post-transplant after HLA desensitization.
Abstract Background Acute allograft rejection after HLA desensitization is common early post‐transplant but the sequence of histopathologic changes leading to graft dysfunction has not been well defined. Methods We evaluated the early pathogenesis and sequence of antibody‐mediated graft damage of 35 desensitized living donor kidney recipients by studying the course of biopsies taken in the very early post‐transplant period (<1 month). Results A total of 14 of the 35 patients met criteria for acute antibody‐mediated rejection ( AMR ). In these patients, the chronologic sequence of pathologic changes was C 4d peritubular capillary deposition, acute tubular injury, and peritubular capillaritis, followed by glomerulitis and interstitial inflammation. Classic AMR lesions occurred early, followed by mononuclear cellular infiltration, which comprised CD 4 and CD 8 T cells and monocytes. Development of graft dysfunction in most patients occurred concurrently with the emergence of graft cellular infiltration, rather than at the earlier time of antibody deposition as detected via C 4d deposition. Conclusion These data provide novel insight into the sequence of pathologic changes in patients with AMR post‐transplant after HLA desensitization.
Background Acute allograft rejection after HLA desensitization is common early post‐transplant but the sequence of histopathologic changes leading to graft dysfunction has not been well defined. Methods We evaluated the early pathogenesis and sequence of antibody‐mediated graft damage of 35 desensitized living donor kidney recipients by studying the course of biopsies taken in the very early post‐transplant period (<1 month). Results A total of 14 of the 35 patients met criteria for acute antibody‐mediated rejection (AMR). In these patients, the chronologic sequence of pathologic changes was C4d peritubular capillary deposition, acute tubular injury, and peritubular capillaritis, followed by glomerulitis and interstitial inflammation. Classic AMR lesions occurred early, followed by mononuclear cellular infiltration, which comprised CD4 and CD8 T cells and monocytes. Development of graft dysfunction in most patients occurred concurrently with the emergence of graft cellular infiltration, rather than at the earlier time of antibody deposition as detected via C4d deposition. Conclusion These data provide novel insight into the sequence of pathologic changes in patients with AMR post‐transplant after HLA desensitization.
Author Yu, Z.
Hadley, G.A.
Sun, Q.
DiPaola, N.R.
Henry, M.
Satoskar, A.
Singh, N.
Winters, H.
Nadasdy, T.
Pelletier, R.P.
Adams, P.
Pesavento, T.
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CitedBy_id crossref_primary_10_1016_j_phrs_2017_12_032
crossref_primary_10_1111_ajt_12596
crossref_primary_10_1155_2013_859761
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Snippet Background Acute allograft rejection after HLA desensitization is common early post‐transplant but the sequence of histopathologic changes leading to graft...
Acute allograft rejection after HLA desensitization is common early post-transplant but the sequence of histopathologic changes leading to graft dysfunction...
Abstract Background Acute allograft rejection after HLA desensitization is common early post‐transplant but the sequence of histopathologic changes leading to...
BACKGROUNDAcute allograft rejection after HLA desensitization is common early post-transplant but the sequence of histopathologic changes leading to graft...
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wiley
istex
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Index Database
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StartPage E402
SubjectTerms antibody
desensitization
Desensitization, Immunologic
Flow Cytometry
Follow-Up Studies
Graft Rejection - immunology
Graft Rejection - pathology
HLA
HLA Antigens - immunology
Humans
Isoantibodies - blood
Isoantibodies - immunology
Kidney Transplantation - immunology
Kidney Transplantation - pathology
Prognosis
rejection
renal transplant
Retrospective Studies
Transplantation, Homologous
Title The pathogenesis of acute allograft dysfunction in desensitized renal transplant recipients
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https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1399-0012.2012.01684.x
https://www.ncbi.nlm.nih.gov/pubmed/22882695
https://search.proquest.com/docview/1033455435
Volume 26
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