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Introduction Humoral alloimmunity mediated by donor-specific Human leukocyte antigen (HLA) antibodies (DSAs) is the principal cause of acute and chronic antibody mediated rejection (ABMR) leading to kidney graft damage and having a major impact on graft survival ( Despite a clear association of DSAs with ABMR and poor long term graft outcome, recipients of renal transplants from HLA-identical siblings have been reported to develop accelerated ABMR (5), and immunological graft loss has been observed in DSA-negative patients ( In addition to cell surface antigens, non-HLA antibodies may recognize cryptic antigens that become exposed after tissue damage prompted by ischemia-reperfusion, alloimmunity, and/or chronic inflammation

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In contrast, AMYRs have high affinity and potency in response to amylin peptides, but weak response to human CT (hCT) 7,8

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