Early critical cortical infarction by anti-angiotensin II type 1 receptor antibody

Abstract

Abstract Rationale: Anti-angiotensin II type 1 receptor antibodies (AT1R-Abs) have been demonstrated to increase the risk of antibody-mediated rejection. We report a case of AT1R-Ab mediated rejection which caused early critical cortical infarction. Patient concerns: A 52-year-old man with end-stage kidney disease underwent preemptive kidney transplantation (KT) from his wife. He had no immunologic risk except ABO incompatibility. Proper desensitization treatment were applied prior to KT. On postoperative day 1, he showed stable clinical course with adequate urine output, but there was no decrease in serum creatinine level and imaging studies showed hypoperfusion in the transplanted kidney. Diagnoses: Allograft biopsy revealed total cortical infarction with severe necrotizing vasculitis, but the medullary area was preserved. Serum AT1R-Ab concentration was elevated from 10.9\u200aU/mL before KT to 19.1\u200aU/mL on 7\u200adays after KT. Interventions: He was treated with plasmapheresis, intravenous immunoglobulin, rituximab, high-dose methylprednisolone, and bortezomib. Outcomes: The treatment showed a partial response, and he was discharged with 7.3\u200amg/dL creatinine level. At 4\u200amonths, his creatinine plateaued at 5.5\u200amg/dL and AT1R-Ab decreased to 3.6\u200aU/mL. Lessons: This case highlights the risk of early active antibody-mediated rejection by preformed AT1R-Ab, suggesting its ability to exhibit atypical histopathologic findings, such as total cortical infarction.