title: Clinicopathological analysis of acute vascular rejection cases after renal transplantation.
abstract: Histopathological change of acute vascular rejection (AVR) is characterized by intimal arteritis and transmural arteritis. In this report, we discuss the clinicopathological analysis of AVR cases after renal transplantation (RTX).
  
  
  METHODS
  AVR was diagnosed in 17 patients from 17 renal transplant patients followed in our institute between January 2003 and September 2008. We retrospectively reviewed these 17 patients.
  
  
  RESULTS
  Among 17 cases of AVR, 10 cases were mild (v1 in Banff 07 classification), five were moderate (v2), and two were severe (v3). Interstitial inflammation (i1-i3) was present in all 17 biopsies. Moderate to severe tubulitis (t2-t3) was present in seven biopsies, and transplant glomerulitis (g1-g3) was present in 11, peritubular capillaritis (ptc1-ptc3) was in 15 of 17 biopsies. C4d deposition in peritubular capillary (PTC) was observed in 6 of 17 cases. By assaying with plastic beads coated with anti-human leukocyte antigen (HLA) antigen performed in 17 cases, the circulating ant-HLA alloantibody was detected in 10 patients, of which 5/10 were donor-specific antibodies (DSA). Acute antibody-mediated rejection (AAMR) was diagnosed in three cases. Many of v1 cases, steroid pulse therapy (SP) were effective. In v2 and v3 cases, six of seven were steroid-resistant rejection and were need more anti-rejection therapy (ART), such as muromonab CD3 (OKT3) injection, gusperimus (DSG) injection, plasmapheresis, intravenous immune globulin, and injection of rituximab. Ten of 17 patients recovered their renal allograft functions by ART, and 16 of 17 patients' grafts are functioning. Deterioration of renal allografts' function after biopsies was seen in seven patients with one of them lost their graft.
  
  
  CONCLUSIONS
  In some cases, AVR might be provoked by anti-donor antibodies. The prognosis of the graft exhibiting AVR was relatively good in present immunosuppression and ART.
authors.affiliation: Department of Urology, Tokyo Women's Medical University, Tokyo, Japan. houichi@aol.com
authors.forename: Tomokazu
authors.initials: T
authors.lastname: Shimizu
authors.forename: Hideki
authors.initials: H
authors.lastname: Ishida
authors.forename: Hiroki
authors.initials: H
authors.lastname: Shirakawa
authors.forename: Kazuya
authors.initials: K
authors.lastname: Omoto
authors.forename: Kuniko
authors.initials: K
authors.lastname: Tsunoyama
authors.forename: Tadahiko
authors.initials: T
authors.lastname: Tokumoto
authors.forename: Kazunari
authors.initials: K
authors.lastname: Tanabe
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D001167:Arteritis / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D001323:Autoantibodies / Q000097:blood; D015935:Complement C4b / Q000378:metabolism; D005260:Female; D005921:Glomerulonephritis / Q000473:pathology; D006084:Graft Rejection / Q000209:etiology / Q000473:pathology*; D006801:Humans; D016030:Kidney Transplantation / Q000009:adverse effects* / Q000276:immunology; D007684:Kidney Tubules / Q000473:pathology; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000378:metabolism; D011379:Prognosis; D012077:Renal Artery / Q000473:pathology*; D012189:Retrospective Studies; D017539:Tunica Intima / Q000378:metabolism / Q000473:pathology*; D055815:Young Adult
chemical_list: D001323:Autoantibodies; D010446:Peptide Fragments; D015935:Complement C4b; C032261:complement C4d