Publication: Successful Treatment of Anti–angiotensin II Type 1 Receptor Antibody–Associated Rejection in Kidney Transplantation: A Case Report
Issued Date
2018-04-01
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ISSN
18732623
00411345
00411345
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2-s2.0-85040366476
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Mahidol University
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SCOPUS
Bibliographic Citation
Transplantation Proceedings. Vol.50, No.3 (2018), 877-880
Suggested Citation
P. Wiwattanathum, A. Ingsathit, D. Thammanichanond, S. Worawichawong Successful Treatment of Anti–angiotensin II Type 1 Receptor Antibody–Associated Rejection in Kidney Transplantation: A Case Report. Transplantation Proceedings. Vol.50, No.3 (2018), 877-880. doi:10.1016/j.transproceed.2017.11.027 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/46779
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Title
Successful Treatment of Anti–angiotensin II Type 1 Receptor Antibody–Associated Rejection in Kidney Transplantation: A Case Report
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Abstract
© 2017 Elsevier Inc. Angiotensin II type 1 receptor (AT1R) antibody, a non-HLA antibody, has been found to have a detrimental effect on kidney allografts. Similarly to HLA antibodies, recipients who have AT1R antibodies are at risk for allograft rejection and poor long-term graft outcome. Besides mediating allograft rejections via direct effects on endothelial and vascular smooth muscle without complement activation, AT1R antibodies may lead to accelerated hypertension via the renin-angiotensin pathway. There has been no definite level of AT1R antibody that predicts allograft rejection. Because of a low incidence of AT1R antibody–associated rejection, there are few reports on specific treatment. The results of conventional treatment, which aims to remove these pathologic antibodies similarly to the treatment of HLA antibody–associated rejection, have been unsatisfactory. Some studies recommend using angiotensin receptor blocker to attenuate the adverse effects of AT1R antibody on kidney allograft. Herein we present a kidney transplant recipient with AT1R antibody–associated refractory allograft rejection who was successfully treated with the use of steroid, plasmapheresis, intravenous immunoglobulin, and rituximab.