Clinical Impact of Pre-transplant Antibodies Against Angiotensin II Type I Receptor and Major Histocompatibility Complex Class I-Related Chain A in Kidney Transplant Patients.
10.3343/alm.2018.38.5.450
- Author:
Ji Won MIN
1
;
Hyeyoung LEE
;
Bum Soon CHOI
;
Cheol Whee PARK
;
Chul Woo YANG
;
Yong Soo KIM
;
Yeong Jin CHOI
;
Eun Jee OH
;
Byung Ha CHUNG
Author Information
1. Division of Nephrology, Department of Internal Medicine, Bucheon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Bucheon, Korea.
- Publication Type:Original Article
- Keywords:
Angiotensin II type 1 receptor;
Donor-specific anti-HLA antibody;
Microvascular inflammation;
Kidney transplantation
- MeSH:
Allografts;
Angiotensin II*;
Angiotensins*;
Antibodies*;
Humans;
Inflammation;
Kidney Transplantation;
Kidney*;
Major Histocompatibility Complex*;
Receptor, Angiotensin, Type 1;
Retrospective Studies;
Risk Factors
- From:Annals of Laboratory Medicine
2018;38(5):450-457
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Evidence of antibody-mediated injury in the absence of donor-specific HLA antibodies (HLA-DSA) has recently emerged, suggesting a role of antibodies in targeting non-HLA antigens expressed on renal allograft tissue. However, the clinical significance of pre-transplant non-HLA antibodies remains unclear. We compared the histological and clinical impact of pre-transplant HLA-DSA and non-HLA antibodies, especially angiotensin II type I receptor (anti-AT1R) and MHC class I-related chain A (anti-MICA), in kidney transplant patients. METHODS: Pre-transplant HLA-DSA, anti-AT1R, and anti-MICA were retrospectively examined in 359 kidney transplant patients to determine the effect of each antibody on allograft survival and clinical characteristics. RESULTS: Pre-transplant HLA-DSA, anti-AT1R, and anti-MICA were detected in 37 (10.3%), 174 (48.5%), and 50 patients (13.9%), respectively. Post-transplant antibody-mediated rejection was associated with a pre-transplant HLA-DSA (+) status only. The development of microvascular inflammation (MVI) was associated with pre-transplant HLA-DSA (P=0.001) and anti-AT1R (P=0.036). Anti-AT1R (+) patients had significantly lower allograft survival compared with anti-AT1R (−) patients (P=0.042). Only pre-transplant anti-AT1R positivity was an independent risk factor for allograft failure (hazard ratio 4.824, confidence interval 1.017–24.888; P=0.038). MVI was the most common histological feature of allograft failure in patients with pre-transplant anti-AT1R. CONCLUSIONS: Pre-transplant anti-AT1R is an important risk factor for allograft failure, which may be mediated by MVI induction in the allograft tissue.
