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Kidney Week

Abstract: PO2202

Regardless of Donor-Specific Antibody, Do Not Forget Non-HLA

Session Information

Category: Transplantation

  • 1902 Transplantation: Clinical

Authors

  • Wysocki, Matthew Stephen, Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Schaefer, Heidi M., Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Shawar, Saed, Vanderbilt University Medical Center, Nashville, Tennessee, United States
Introduction

Antibody-Mediated Rejection (AMR) remains an important cause of allograft rejection and loss of transplant. This is mainly attributed to donor-specific antibodies (DSA) directed against human leukocyte antigen (HLA). In patients with biopsy findings of AMR and undetectable DSA, non-HLA antibodies must be considered. Here we present two cases of AMR mediated by Angiotensin II type 1 receptor (AT1R) antibody, one of the most widely studied non-HLA antibodies.

Case Description

A 46 yo AA HIV-positive male underwent deceased donor kidney transplant, induced with Basiliximab and methylprednisolone, and maintained on tacrolimus, mycophenolate mofetil and prednisone. His post-op course was complicated by delayed graft function with biopsy performed on day 11 showing acute vascular rejection and severe microcirculation inflammation, highly suspicious for AMR. DSA was negative, but non-HLA panel resulted positive for anti-AT1R at 22 U/ml. He was treated with steroids, PLEX, IVIG, Rituximab, and started on ARB therapy with recovery and most recent creatinine 1.59 mg/dl. To our knowledge, this is the first reported case of an HIV-positive patient with anti-AT1R AMR.

A 50 yo AA female underwent deceased donor kidney transplant induced with Alemtuzumab and methylprednisolone and maintained on tacrolimus, mycophenolate mofetil and prednisone. She had immediate graft function, but 5 days after discharge, presented with anuric AKI. Biopsy on day 10 showed thrombotic microangiopathy and diffuse C4d positivity, suggestive of AMR. DSA panel showed MFI values that correlated with high levels of anti-B18 and anti-B25. Non-HLA panel was positive for anti-AT1R at 29 U/ml. She was treated with steroids, PLEX, IVIG, Rituximab, and started on ARB therapy with recovery and most recent creatinine 1.23 mg/dl.

Discussion

Non-HLA antibodies including anti-AT1R have been recognized as possible mediators of allograft injury. They should be suspected in AMR with no identifiable DSA, or in early AMR regardless of DSA. Although no standardized treatment exists for non-HLA antibodies, early recognition may have implications for treatment, particularly with AT1R antibodies in which angiotensin receptor blockade effectively reduces anti-AT1R activity. Along with other AMR therapies, this may improve allograft function as seen in these two cases. To our knowledge, this is the first reported case of an HIV-positive patient with anti-AT1R AMR.