Abstract: TH-PO0938
Timely Treatment Is Key: Management of Antiendothelial Cell Antibody-Mediated Rejection in Kidney Transplant
Session Information
- Transplantation: Clinical - Glomerular Diseases, Infections, and Rejection
November 06, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2102 Transplantation: Clinical
Authors
- Nemalidinne, Krishna Vani, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
- Vanteru, Abinay Siva kumar Reddy, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
- Chevireddy, Akshara, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
- Manchala, Venkata, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
Introduction
The precise identification of kidney transplant rejection caused by non-HLA antibodies remains challenging. However, emerging research suggests that these antibodies contribute to rejection episodes. Here, we present a case of a 48-year-old female managed for rejection mediated by anti-endothelial cell antibodies (AECA).
Case Description
A 48 Y/o female with ESKD from diabetic nephropathy underwent DCD kidney transplantation. She received induction immunosuppression with ATG 4.5 mg/Kg and IV methyl prednisolone. Maintenance immunosuppression with tacrolimus and mycophenolate mofetil (MMF) was initiated. Within 2 weeks post-transplant, she developed AKI with Cr rise from 3.5 to 4.7 mg/dl. AKI workup did not reveal any prerenal or post-renal causes. Hence, a transplant kidney biopsy was done that showed Banff 2A acute T Cell mediated rejection (TCMR), marked microvascular inflammation (g3, ptc3), suggestive of antibody-mediated rejection (ABMR) with negative C4d staining on immunofluorescence. Donor-specific HLA antibodies (DSA) were negative. Non-HLA antibodies, such as Anti-endothelial cell antibodies (AECA), Angiotensin II Type 1 Receptor (AT1R) antibodies, major histocompatibility complex class I polypeptide-related sequence A (MICA) antibodies, were sent out and initiated on treatment with IV pulse steroids and ATG. High index of suspicion remained for ABMR, and hence, we initiated treatment with IVIG and plasmapheresis. A week later, the endothelial cell cross-match median channel shift (MCS) was elevated at 196 (>50 MCS is positive), while the rest were negative. She is maintained on tacrolimus, MMF, and prednisone. Patient’s creatinine improved to 1.1mg/dL within a month of treatment.
Discussion
Non-HLA antibodies are increasingly recognized as contributors to early and recurrent rejection, even in HLA-identical cases. Historically, the absence of diagnostic assays limited their detection, but newer tests now highlight their clinical relevance. ABMR in the absence of DSAs and negative C4d staining should raise suspicion for non-HLA antibody involvement. Early and aggressive immunosuppression is crucial, as these rejections are often severe and recurrent. Due to a 7–14 day delay in non-HLA antibody test results, early empirical treatment is recommended to prevent irreversible graft damage.