Issues remain in the diagnosis of active antibody-mediated rejection (ABMR) in human kidney transplantation, as the hallmark criteria, the microcirculation inflammation scores and the C4d deposits, still lack reproducibility and sensitivity respectively. Using laser microdissection combined with mass spectrometry-based proteomics, this study presents the characterization of active antibody-mediated glomerular injuries, marked by evidences of leukocyte activation and migration, cellular stress through type I and II interferons and of microcirculation remodeling.