ABO incompatibility in DSA-high group was significantly lower. first biopsies, and half of the SAABMR cases developed de novo circular peritubular capillary multilayering in the follow-up biopsies. Conclusion PAABMR was mainly found by the protocol biopsy. The short-term follow-up of SAABMR patients did not show worsening clinically and light microscopically, but ultrastructural examination by EM was useful to detect early lesions of endothelial injury and progression of glomerular and peritubular capillary basement membrane alterations. Keywords: Acute/active antibody-mediated rejection, Allograft, Banff 2013 classification, Electron microscopy, Kidney transplantation Introduction The pathological diagnostic criteria for acute/active antibody-mediated rejection (AABMR) were revised at the Banff 2013 meeting [1]. According to this meeting report, histological evidence of acute tissue injury, evidence of an interaction between antibodies and the vascular endothelium, and serological evidence of donor-specific antibodies (DSAs) are essential for the diagnosis of AABMR. In addition, evaluation by both electron microscopy (EM) and light microscopy (LM) is required to exclude chronic lesions in patients with chronic antibody-mediated rejection [1]. Haas and Mirocha [2] reported a trend toward a lower incidence of developing overt transplant glomerulopathy in recipients who were treated for moderate microvascular inflammation (+ ptc 2) in the presence of DSAs than in those who were untreated. In another study, recipients with antibody-mediated rejection showed a significantly higher DSA mean fluorescence intensity (MFI) [3]. However, the MFI cutoff value for DSAs is not defined in the Banff 2013 classification [1]. Several reports have argued the significance of EM evaluation to diagnose AABMR. Wavamunno et al. [4] reported that endothelial and subendothelial ultrastructural abnormalities in glomeruli are early markers of transplant glomerulopathy. Haas and Mirocha [2] reported that ultrastructural changes, including glomerular endothelial swelling, subendothelial widening, and early glomerular basement membrane (GBM) duplication, were detected in biopsy specimens (BS) of antibody-mediated rejection patients within 3 months. At the Banff 2013 meeting, evaluation of early chronic cg lesions by EM was determined to be required [1]. However, the relationship between EM and clinical findings has not been fully elucidated. The aim of this study was to evaluate the clinicopathological BMS-813160 features and activity of AABMR and subsequent early chronic lesions, like duplication of GBM and multilayering of peritubular capillary basement membrane (PTCBM), BMS-813160 according to the Banff 2013 classification [1]. Materials and Methods Patients Protocol biopsies at Toho University Omori Medical Center are usually performed at 1 hour, 3 months, 1 year, 3 years, and 7 F2RL3 years, and, for some recipients, 10 years after transplantation. We cross-sectionally analyzed 345 BS of 269 kidney transplant recipients performed at Toho University Omori Medical Center from January 2016 to December BMS-813160 2017. Among the recipients diagnosed with subclinical AABMR (SAABMR) by the protocol biopsy from January 2016 to December 2017, we evaluated the clinical and histological changes of recipients in whom follow-up BS evaluable by EM was performed until June 2018. The basic regimen of immunosuppressive therapy at Toho University Omori Medical Center included methylprednisolone, mycophenolate mofetil or azathioprine, tacrolimus (Tac) or cyclosporine (CsA), basiliximab, and anti-thymocyte globulin for preformed DSA cases. Histopathology Histological evaluation of allograft biopsies at Toho University Omori Medical Center was performed by hematoxylin and eosin, periodic acid-Schiff, periodic acid methenamine silver, and Masson trichrome staining. Histological evidence of acute tissue injury, evidence of an interaction between antibodies and the vascular endothelium, and serological evidence of DSAs were essential to diagnose AABMR BMS-813160 according to the Banff 2013 classification, and evaluation by both EM and LM was required to exclude early chronic lesions like GBM duplication and multilayering of PTCBM with chronic antibody-mediated rejection [1]. In the present study, we defined a biopsy finding of AABMR (pathological AABMR [PAABMR]) as histological evidence of acute tissue injury and endothelial injury (microvascular inflammation identified by LM or C4d deposition in peritubular capillaries identified by immunohistochemistry). We defined a biopsy finding of PAABMR as relevant findings by only LM regardless of the presence of DSAs. The presence of DSAs was determined using the LABScreen Single Antigen test. We defined an MFI of 1 1,000 as DSA positivity in accordance with the cutoff.