title: Pathologic features of antibody-mediated rejection in renal allografts:  an expanding spectrum.
abstract: OBJECTIVE
  This review discusses recent findings that are changing and expanding the spectrum of pathologic changes associated with antibodies directed against renal allografts.
  
  
  RESULTS
  This review focuses on four lesions: subclinical antibody-mediated rejection (AMR), C4d-negative AMR, intimal arteritis, and arterial intimal fibrosis. A number of studies have identified morphologic lesions of AMR in protocol biopsies of normally functioning renal allografts, particularly in sensitized recipients, that correlate with subsequent development of chronic changes in the graft, including transplant glomerulopathy. These same studies as well as molecular studies of indication biopsies of conventional renal allografts have noted evidence of microvascular injury, which, in the presence of donor-specific antibodies (DSAs) but the absence of C4d deposition in peritubular capillaries, is associated with development of transplant glomerulopathy and graft loss. Finally, recent studies suggest that intimal arteritis, previously felt to represent a lesion of cell-mediated rejection, and bland arterial intimal fibrosis, resembling arteriosclerosis, may in some cases be manifestations of DSA-induced graft injury.
  
  
  CONCLUSIONS
  Incorporation of these newly recognized lesions of AMR into a working diagnostic schema with sufficient sensitivity and specificity to minimize undertreatment and overtreatment of patients is an important challenge currently faced by renal pathologists and transplant clinicians.
authors.affiliation: Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, California 91403, USA. mark.haas@cshs.org
authors.forename: Mark
authors.initials: M
authors.lastname: Haas
mesh_terms: D000818:Animals; D001167:Arteritis / Q000276:immunology / Q000473:pathology; D001706:Biopsy; D015935:Complement C4b / Q000276:immunology; D005355:Fibrosis; D006084:Graft Rejection / Q000145:classification / Q000276:immunology* / Q000473:pathology*; D006085:Graft Survival; D006801:Humans; D007518:Isoantibodies / Q000276:immunology*; D007668:Kidney / Q000098:blood supply / Q000276:immunology* / Q000473:pathology*; D016030:Kidney Transplantation / Q000276:immunology*; D010446:Peptide Fragments / Q000276:immunology; D012077:Renal Artery / Q000276:immunology / Q000473:pathology; D016896:Treatment Outcome; D017539:Tunica Intima / Q000276:immunology / Q000473:pathology
chemical_list: D007518:Isoantibodies; D010446:Peptide Fragments; D015935:Complement C4b; C032261:complement C4d