Conflict of interest: The authors have no conflict of interest to declare.
Clinicopathological analysis of acute vascular rejection cases after renal transplantation
Article first published online: 7 JUN 2010
© 2010 John Wiley & Sons A/S
Special Issue: Proceedings of the 13th Clinicopathological Conference on Renal Allograft Pathology, 18 July 2009, Tokyo, Japan
Volume 24, Issue Supplement s22, pages 22–26, July 2010
How to Cite
Shimizu, T., Ishida, H., Shirakawa, H., Omoto, K., Tsunoyama, K., Tokumoto, T. and Tanabe, K. (2010), Clinicopathological analysis of acute vascular rejection cases after renal transplantation. Clinical Transplantation, 24: 22–26. doi: 10.1111/j.1399-0012.2010.01277.x
- Issue published online: 7 JUN 2010
- Article first published online: 7 JUN 2010
- Accepted for publication 26 February 2010
- acute vascular rejection;
- intimal arteritis;
- renal transplantation;
- transmural arteritis
Shimizu T, Ishida H, Shirakawa H, Omoto K, Tsunoyama K, Tokumoto T, Tanabe K. Clinicopathological analysis of acute vascular rejection cases after renal transplantation. Clin Transplant 2010: 24 (Suppl. 22): 22–26. © 2010 John Wiley & Sons A/S.
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).
Patients: 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.