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Abstract: SA-PO1199

Late-Onset Antibody-Mediated Rejection Nine Years After Kidney Transplantation

Session Information

Category: Transplantation

  • 2002 Transplantation: Clinical

Authors

  • Safi, Adnan, SUNY Downstate Health Sciences University, New York, New York, United States
  • Suraj, Fnu, SUNY Downstate Health Sciences University, New York, New York, United States
  • Lwin, Yone Mee Mee, SUNY Downstate Health Sciences University, New York, New York, United States
  • Nenwani, Hari Vishal, SUNY Downstate Health Sciences University, New York, New York, United States
  • Akatibo, Emmanuel, SUNY Downstate Health Sciences University, New York, New York, United States
  • Kouyate, Gnama, SUNY Downstate Health Sciences University, New York, New York, United States
  • Syed, Jahanghir, SUNY Downstate Health Sciences University, New York, New York, United States
  • Roche-Recinos, Andrea, SUNY Downstate Health Sciences University, New York, New York, United States
  • Yang, Yihe, Weill Cornell Medicine, New York, New York, United States
  • Salifu, Moro O., SUNY Downstate Health Sciences University, New York, New York, United States
  • Saggi, Subodh J., SUNY Downstate Health Sciences University, New York, New York, United States
Introduction

Antibody-mediated rejection remains a major cause of late kidney allograft dysfunction and loss. De novo donor-specific antibodies, particularly complement-binding class II antibodies, may emerge years after transplant and cause subclinical injury despite stable renal function.

Case Description

A 62-year-old man with ADPKD underwent deceased donor kidney transplant in February 2016, with immediate graft function (best creatinine: 1.4 mg/dL). In 2016, transient Class I DSA was detected without biopsy-proven rejection and renal artery stenosis was treated with angioplasty, after which creatinine stabilized at 1.6–1.8 mg/dL. From 2016 to May 2024, graft function remained stable without proteinuria, infection, or AKI, and DSA remained negative. In March 2025, after missing several follow-ups, he presented asymptomatically with a creatinine of 1.6 mg/dL but was found to have a reappearance of complement-binding Class II DSA (DQB103:02/DQA103:01, MFI 14,201, C3d positive). Donor-derived cfDNA was elevated at 1.3%. Kidney allograft biopsy in May 2025 showed active ABMR with glomerulitis (g2), peritubular capillaritis (ptc2), and diffuse C4d positivity, without T-cell-mediated rejection. Mycophenolate mofetil was increased, tacrolimus was titrated to a trough of 8.1 ng/mL, and prednisone was continued. By June 2025, DSA increased to 22,673 MFI despite stable creatinine and no proteinuria.

Discussion

Late-onset ABMR may occur years after transplant despite stable creatinine. Re-emergent complement-binding Class II dnDSA, elevated dd-cfDNA, and biopsy-proven microvascular injury indicate ongoing subclinical alloimmune damage. Lifelong surveillance, immunosuppression adherence, and timely biopsy are key to preserving graft survival.