title: Rejection of the Renal Allograft in the Absence of Demonstrable Antibody and Complement.
abstract: Recent literature has stressed the prominent role of antibodies in graft loss. This study was designed to assess a growing perception that T cell-mediated rejection (TCMR) is no longer clinically relevant.
  
  
  
  Five hundred forty-five renal allograft recipients over a 3-year period were screened for biopsies with: (a) TCMR including borderline change (BL), (b) negative complement protein C4 degradation fragment, and (c) absence of donor-specific antibody at time of transplant, within 30 days of the biopsy, and up to 4 measurements at later time points.
  
  
  
  These stringent requirements identified 28 "pure" cases of late TCMR/BL. Low-grade glomerulitis, peritubular capillaritis, or chronic transplant glomerulopathy were found in 9/28 (32%) biopsies. Serum creatinine showed complete short-term remission in 7/10 (70%) BL and 9/18 (50%) TCMR patients 1 month postbiopsy. Yet, both treated and untreated patients demonstrated further decline in graft function as assessed by serum creatinine and estimated glomerular filtration rate.
  
  
  
  Late TCMR seen in 7.9% of biopsies can contribute to significant deterioration of graft function in patients in whom the dominant contribution of antibody-mediated injury has been reasonably excluded. Our data also reinforce existing literature showing that microvascular lesions do not have absolute specificity for a diagnosis of antibody-mediated rejection.
authors.affiliation: 1 Department of General Surgery, Beijing Friendship Hospital, Capital Medical University, Beijing, China. 2 Department of Organ Transplantation, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. 3 Department of Pathology, The Thomas E Starzl Transplantation Institute, University of Pittsburgh, School Of Medicine, Pittsburgh, PA.
authors.forename: Xiaomu
authors.initials: X
authors.lastname: Zhao
authors.forename: Gang
authors.initials: G
authors.lastname: Huang
authors.forename: Simrath
authors.initials: S
authors.lastname: Randhawa
authors.forename: Gang
authors.initials: G
authors.lastname: Zeng
authors.forename: John
authors.initials: J
authors.lastname: Lunz
authors.forename: Parmjeet
authors.initials: P
authors.lastname: Randhawa
mesh_terms: D000328:Adult; D000368:Aged; D064591:Allografts; D015415:Biomarkers / Q000097:blood; D001706:Biopsy; D016022:Case-Control Studies; D015935:Complement C4b / Q000032:analysis*; D003404:Creatinine / Q000097:blood; D005260:Female; D005355:Fibrosis; D006084:Graft Rejection / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy / Q000276:immunology*; D006085:Graft Survival; D006680:HLA Antigens / Q000276:immunology*; D006801:Humans; D007111:Immunity, Cellular / Q000187:drug effects; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007518:Isoantibodies / Q000097:blood*; D007668:Kidney / Q000187:drug effects / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D016030:Kidney Transplantation / Q000009:adverse effects*; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000032:analysis*; D012307:Risk Factors; D013601:T-Lymphocytes / Q000276:immunology*; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D006680:HLA Antigens; D007166:Immunosuppressive Agents; D007518:Isoantibodies; D010446:Peptide Fragments; D015935:Complement C4b; C032261:complement C4d; D003404:Creatinine