Intro: Donor specific antibodies (DSAs) detected post transplant are associated with ABMR and graft dysfunction. The role of non-HLA antibodies especially angiotensin II receptor type I antibodies (AT1R) is unclear. It has been suggested that post- transplant development of AT1R antibodies can result in malignant hypertension, acute ABMR, graft thrombosis and failure (Reinsmoen NL. Hum Immunol.2013 Nov; 74(11):1474-7). Here, we examined histologic features of biopsies from pediatric patients with strong AT1R antibodies (group 1) and compared them to patients with DSA and AT1R (group 2), and those with DSA alone (group 3). Methods: From August 2015, we identified 9 pediatric post transplant patients who had routine DSA and AT1R testing done. Patients who had strong DSA (>10,000MFI) and/or Strong AT1R antibodies (>17units/ml) underwent a renal biopsy. There were 3 patients in each group. All patients had stable renal function at the time of biopsy. Scoring of the biopsy was by Banff criteria. Results: Patients in Group 1 did not have pathologic features of ABMR. All 3 patients in Group 2 had active ABMR. 2/3 patients in Group 2 also had concomitant cell mediated rejection (CMR). The g +ptc scores and cg scores were higher in Group 2 and 3, however Group 1 had greater IFTA scores compared to group 2 and 3. See figure 1 & 2. Conclusion: From our experience with isolated AT1R antibody positivity, we do not see manifestations of active ABMR on renal biopsies. However, the presence of DSAs is closely a/w ABMR, with or without AT1R. Patients with DSA + AT1R have concomitant CMR. Thus, the role of AT1R antibodies in mediation of ABMR is questionable. Immune responses to AT1R may be allotypic in nature and may not cross react with donor AT1R.

CITATION INFORMATION: Choi J, Haas M, Zhang X, Aubert O, Pizzo H, Kamil E, Irene K, Jordan S, Puliyanda D. Isolated Angiotensin II Receptor Type I Antibodies (AT1R) Are Not Associated with Active Antibody Mediated Rejection (ABMR) in Pediatric Renal Transplant Recipients. Am J Transplant. 2017;17 (suppl 3).

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