title: Antibody-mediated vascular rejection of kidney allografts: a population-based study.
abstract: BACKGROUND
  Rejection of allografts has always been the major obstacle to transplantation success. We aimed to improve characterisation of different kidney-allograft rejection phenotypes, identify how each one is associated with anti-HLA antibodies, and investigate their distinct prognoses.
  
  
  METHODS
  Patients who underwent ABO-compatible kidney transplantations in Necker Hospital and Saint-Louis Hospital (Paris, France) between Jan 1, 1998, and Dec 31, 2008, were included in our population-based study. We assessed patients who provided biopsy samples for acute allograft rejection, which was defined as the association of deterioration in function and histopathological lesions. The main outcome was kidney allograft loss-ie, return to dialysis. To investigate distinct rejection patterns, we retrospectively assessed rejection episodes with review of graft histology, C4d in allograft biopsies, and donor-specific anti-HLA antibodies.
  
  
  RESULTS
  2079 patients were included in the main analyses, of whom 302 (15%) had acute biopsy-proven rejection. We identified four distinct patterns of kidney allograft rejection: T cell-mediated vascular rejection (26 patients [9%]), antibody-mediated vascular rejection (64 [21%]), T cell-mediated rejection without vasculitis (139 [46%]), and antibody-mediated rejection without vasculitis (73 [24%]). Risk of graft loss was 9·07 times (95 CI 3·62-19·7) higher in antibody-mediated vascular rejection than in T cell-mediated rejection without vasculitis (p<0·0001), compared with an increase of 2·93 times (1·1-7·9; P=0·0237) in antibody-mediated rejection without vasculitis and no significant rise in T cell-mediated vascular rejection (hazard ratio [HR] 1·5, 95% CI 0·33-7·6; p=0·60).
  
  
  CONCLUSIONS
  We have identified a type of kidney rejection not presently included in classifications: antibody-mediated vascular rejection. Recognition of this distinct phenotype could lead to the development of new treatment strategies that could salvage many kidney allografts.
  
  
  BACKGROUND
  None.
authors.affiliation: Nephrology and Kidney Transplantation, Saint-Louis Hospital, Assistance Publique Hôpitaux de Paris, INSERM U940, Paris, France.
authors.forename: Carmen
authors.initials: C
authors.lastname: Lefaucheur
authors.forename: Alexandre
authors.initials: A
authors.lastname: Loupy
authors.forename: Dewi
authors.initials: D
authors.lastname: Vernerey
authors.forename: Jean-Paul
authors.initials: JP
authors.lastname: Duong-Van-Huyen
authors.forename: Caroline
authors.initials: C
authors.lastname: Suberbielle
authors.forename: Dany
authors.initials: D
authors.lastname: Anglicheau
authors.forename: Jérôme
authors.initials: J
authors.lastname: Vérine
authors.forename: Thibaut
authors.initials: T
authors.lastname: Beuscart
authors.forename: Dominique
authors.initials: D
authors.lastname: Nochy
authors.forename: Patrick
authors.initials: P
authors.lastname: Bruneval
authors.forename: Dominique
authors.initials: D
authors.lastname: Charron
authors.forename: Michel
authors.initials: M
authors.lastname: Delahousse
authors.forename: Jean-Philippe
authors.initials: JP
authors.lastname: Empana
authors.forename: Gary S
authors.initials: GS
authors.lastname: Hill
authors.forename: Denis
authors.initials: D
authors.lastname: Glotz
authors.forename: Christophe
authors.initials: C
authors.lastname: Legendre
authors.forename: Xavier
authors.initials: X
authors.lastname: Jouven
mesh_terms: D015704:CD4 Antigens / Q000032:analysis; D004692:Endarteritis / Q000276:immunology; D005260:Female; D006084:Graft Rejection / Q000276:immunology* / Q000473:pathology; D006680:HLA Antigens / Q000276:immunology*; D006801:Humans; D007518:Isoantibodies / Q000097:blood*; D016030:Kidney Transplantation / Q000276:immunology*; D008297:Male; D008875:Middle Aged
chemical_list: D015704:CD4 Antigens; D006680:HLA Antigens; D007518:Isoantibodies