The association between anti-AT1Rabs and microvascular injury observed in antibody-mediated rejection has been described in kidney graft Biopsies (KGBx). We herein describe the histopathologic findings of KGBx performed during the first year of transplantation (Tx) in 134 patients tested for pre-Tx anti-AT1Rabs in cryopreserved sera (04/2009 to 09/2013). Protocol KGBx before implantation (time-zero), 1 year after Tx and for cause KGBx were included. 21/134 Tx patients were anti-AT1Rab positive (≥17 U/mL); 7/21 experienced acute rejection. For comparison a control group with anti-AT1Rabs <17 U/mL, with (n = 16) and without (n = 31) acute rejection was included. Preimplantation KGBx showed no differences in inflammatory and chronic findings, nor in subintimal fibrosis (25 vs 12.8%, p =.42) between patients with anti-AT1Rabs ≥17 U/mL and those with <17 U/mL. Follow-up KGBx revealed a significantly greater proportion of arterial sub-intimal fibrosis (52.3 vs. 27.6%, p =.049) and extension (15.7 vs. 5.3, p =.015) in anti-AT1Rabs ≥17 U/mL compared to anti-AT1Rabs <17 U/mL KGBx. No differences were observed in microcirculation inflammation, nor in interstitial fibrosis or tubular atrophy between groups. Also, anti-AT1Rabs ≥17 U/mL (β 10.1, 2.3 to 17.8, p =.012) and more importantly anti-AT1Rabs ≥ 30 U/mL (β12.1, 3.1 to 20.9, p <.01), were independent risk factors associated with vascular occlusion resulting from sub-intimal fibrosis. Our study findings have shown that anti-AT1Rab values ≥17 U/mL are significantly associated to sub-intimal fibrosis and a greater percentage of vessel occlusion in kidney graft biopsies obtained during the first year posttransplant, particularly in coexistence with inflammation and de novo DSA. • Patients with anti-AT1Rabs ≥17 U/mL had greater arterial sub-intimal fibrosis • Anti-AT1Rabs ≥17 U/mL and ≥ 30 U/mL are associated with vascular occlusion • Anti-AT1Rabs ≥17 U/mL is not associated to microcirculation inflammation • Anti-AT1Rabs ≥17 U/mL is not related to interstitial fibrosis or tubular atrophy [ABSTRACT FROM AUTHOR]