Contents lists available at ScienceDirect Transplant Immunology journal homepage: www.elsevier.com/locate/trim Antibody mediated rejection due to de-novo DSA causing venous thrombosis of pancreas allograft – A case report Kunal Yadav a, ⁎ , Adrian Cotterell a , Pamela Kimball a , Laura Warmke b , Melissa Contos b , Gaurav Gupta c , Anne King c , Dhiren Kumar c , Marlon Levy a a Division of Transplantation, Department of Surgery, Virginia Commonwealth University, Richmond, VA, United States b Department of Pathology, Virginia Commonwealth University, Richmond, VA, United States c Division of Nephrology, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, United States ABSTRACT This case describes a 34 year old female who underwent an HLA identical living donor kidney transplant with a positive flow cytometric crossmatch (FCXM), but without any donor specific antibody (DSA). Tests to detect non- HLA antibody and autoantibody were negative. Allograft functioned well without rejection. She later received a pancreas allograft, again with a weakly positive FCXM, without DSA. After good initial graft function, she developed hyperglycemia six weeks posttransplant. Cross-sectional imaging demonstrated non-enhancing pan- creas allograft with new vein thrombosis. She underwent transplant pancreatectomy, the explant pathology demonstrated changes consistent with severe acute antibody mediated rejection (AMR) causing thrombosis of the pancreas allograft. She had also developed several de-novo class-I DSAs at this time. Despite extensive testing, we could not identify a causative antibody for the initial positive FCXMs or its role in the eventual rejection of the pancreas allograft. 1. Introduction Venous thrombosis is the most common cause of early allograft loss after pancreas transplantation [1]. Even though technical factors are usually implicated as the cause of thrombosis in the early perioperative period, a histopathological analysis of pancreas explants after venous thrombosis has demonstrated that as many as one-third of allograft thromboses can be secondary to rejection [2]. We report an interesting case of a pancreas after kidney (PAK) transplant with positive pretransplant XM without detectable DSA who later developed de-novo DSA, allograft rejection and thrombosis. 2. Case presentation A 34 year old white female with type-1 diabetes mellitus (DM-I) with stage 5 chronic kidney disease (CKD), with a calculated panel reactive antibody (cPRA) of 8% underwent a living donor kidney transplant from her HLA identical brother (HLA – A1,3; B8,62; Bw6; Cw7,10; DR4,13; DRw53,53; DQ6,8; DQA03,10; DPB4,17; DPA01,02). Her prior sensitizations included 4 pregnancies with 2 miscarriages and 2 live births. She had no prior history of blood transfusion or trans- plants. At the time of transplant, complement dependent cytotoxicity crossmatch (CDCXM) was negative, but T and B flow cytometric crossmatches (FCXM) were weakly positive (Table 1). Since there was no identifiable DSA on single antigen bead (SAB) testing, we proceeded with the kidney transplant. The kidney allograft had excellent function. Interestingly, on seri- ally repeating the crossmatch over the next 3–4 years, the FCXM be- came increasingly positive with rising channel shifts and eventually CDCXM also became positive. There was still no DSA. There were no Major-histocompatibility-complex (MHC) class I–related chain A (MICA) antibodies, and low-binding Angiotensin II type-1 receptor (AT1R) antibodies. AutoXM was negative. The FCXM stayed positive after autoadsorption of the patient's serum against her own cells. Treating serum with Dithiotreitol (DTT) to eliminate IgM antibodies, made no change to XM results. All this while, the kidney allograft had stable function without rejection in protocol biopsies. She was listed for a pancreas transplant and received multiple offers over next three years but continued to have positive FCXMs, without DSA. She was subsequently transplanted with a pancreas from a 15 year old brain-dead donor (HLA – A3,23; B37,44; Bw4,4; Cw2,5; DR4,11; DRw52,53; DQ7,7; DQA03,05; DPB1*02:01, 105:01; DPA01,03). Pretransplant CDCXM and T-cell FCXM were negative, but B-cell FCXM was slightly positive; there was no DSA. The pancreas allograft was https://doi.org/10.1016/j.trim.2018.01.001 Received 18 November 2017; Received in revised form 3 January 2018; Accepted 4 January 2018 ⁎ Corresponding author at: Division of Transplantation, Department of Surgery, P.O. Box 980057, Richmond, VA 23298-0057, United States. E-mail address: kunal.yadav@vcuhealth.org (K. Yadav). Transplant Immunology xxx (xxxx) xxx–xxx 0966-3274/ © 2018 Elsevier B.V. All rights reserved. Please cite this article as: Yadav, K., Transplant Immunology (2018), https://doi.org/10.1016/j.trim.2018.01.001