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.
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