title: Plasma cell-rich acute renal allograft rejection.
abstract: BACKGROUND
  Acute renal allograft rejection is usually seen within the first 3 months posttransplant, and is characterized by an intense infiltrate of T cells. Some acute rejections, however, contain many plasma cells and/or appear late posttransplant.
  
  
  METHODS
  We have investigated 27 cases of intensely plasma cell-rich acute rejections (PCAR) from 1987 to 1997 and have compared them to 21 control cases (CAR) of typical acute rejection. Each group was divided into early (<6 months) and late (>6 months) subgroups. PCAR and CAR cases were matched for histological features of chronic allograft nephropathy. In all four groups, most cases had Banff '97 type IB and IIA acute rejection.
  
  
  RESULTS
  A significantly greater number of PCAR cases experienced graft failure due to chronic allograft nephropathy or complications of acute rejection (P<0.05). There was no significant difference between PCAR and CAR in HLA matching, occurrence of posttransplant acute tubular necrosis, presence versus absence of previous allografts, number of previous or subsequent acute rejection episodes, Banff '97 sum scores for acute rejection, cyclosporine A or FK506 levels, or percent change from baseline creatinine at time of biopsy. Plasma cells in PCAR cases showed IgG predominance whereas those in CAR had comparable staining for IgG and IgA. Kappa and lambda light chain immunostaining of all PCAR cases revealed polyclonality. Three of 18 PCAR cases studied for the presence of Epstein-Barr virus RNA showed scattered positivity in 2-7% of lymphoid cells, although the remainder was negative. None of the PCAR cases developed post-transpland lymphoproliferative disorder.
  
  
  CONCLUSIONS
  We conclude that PCAR can occur from 1 month to many years posttransplant, is associated with poor graft survival, and is not a manifestation of concomitant chronic allograft nephropathy or viral infection, including posttransplant lymphoproliferative disorder.
authors.affiliation: Department of Pathology, The Johns Hopkins University, School of Medicine, Baltimore, Maryland 21205-2196, USA.
authors.forename: D A
authors.initials: DA
authors.lastname: Charney
authors.forename: T
authors.initials: T
authors.lastname: Nadasdy
authors.forename: A W
authors.initials: AW
authors.lastname: Lo
authors.forename: L C
authors.initials: LC
authors.lastname: Racusen
mesh_terms: D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D002102:Cadaver; D016572:Cyclosporine / Q000627:therapeutic use; D005260:Female; D006084:Graft Rejection / Q000276:immunology / Q000473:pathology* / Q000517:prevention & control; D006801:Humans; D007150:Immunohistochemistry; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D017403:In Situ Hybridization; D016030:Kidney Transplantation / Q000276:immunology* / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D010950:Plasma Cells / Q000473:pathology*; D016559:Tacrolimus / Q000627:therapeutic use; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D007166:Immunosuppressive Agents; D016572:Cyclosporine; D016559:Tacrolimus