Abstract: FR-PO1227
Post-Transplant Atypical Hemolytic Uremic Syndrome Outcomes with Eculizumab and Ravulizumab: A Single-Center Experience
Session Information
- Transplantation: Clinical - Rejection, Biomarkers, and Pharmacology
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2002 Transplantation: Clinical
Authors
- Gopireddy, Naga Sumanth Reddy, University of Iowa Health Care, Iowa City, Iowa, United States
- Kumar, Abhishek, Yale School of Medicine, New Haven, Connecticut, United States
- Smith, Richard J., University of Iowa Health Care, Iowa City, Iowa, United States
- Nester, Carla M., University of Iowa Health Care, Iowa City, Iowa, United States
- Thomas, Christie P., University of Iowa Health Care, Iowa City, Iowa, United States
Background
Atypical hemolytic uremic syndrome (aHUS) is a complement-mediated thrombotic microangiopathy with high rates of recurrence following kidney transplantation without prophylactic complement inhibition. Eculizumab, a terminal complement inhibitor targeting C5, has transformed post-transplant outcomes, but long-term real-world data remain limited, and experience with transitioning from eculizumab to ravulizumab in the transplant setting is sparse.
Methods
We conducted a retrospective case series of 10 patients with aHUS who received a kidney transplant at our institution and were maintained on eculizumab Q2W, with selective transition to ravulizumab Q8W. Patient demographics, genetic variants, laboratory parameters (hemoglobin, platelets, haptoglobin, LDH, serum creatinine, eGFR), rejection episodes, donor-specific antibodies (DSA), infections, and clinical outcomes were analyzed.
Results
Ten patients (9 female, 1 male) were followed for a median of 122 months (range 40–180). Complement gene variants identified included CFH (n=4), CFI/Factor I (n=3), CFH-CFHR fusion protein (n=1), CFI combined with CFHR3-1 deletion (n=1), and unknown (n=1). Seven patients received living unrelated donor kidneys; three received deceased donor kidneys. Six patients (60%) were transitioned from eculizumab to ravulizumab. One patient experienced graft failure at 40 months due to combined Banff 1B acute cellular rejection and antibody-mediated rejection. One patient died with a functioning graft (eGFR 87) due to pulmonary aspergillosis following high-dose IVIg for AMR. Among the remaining 8 patients with functioning grafts, median eGFR at last follow-up was 69.6 ml/min/1.73m. No patient on continuous eculizumab or ravulizumab experienced confirmed aHUS recurrence. All patients who transitioned to ravulizumab maintained stable complement inhibition without breakthrough Thrombotic Micro Angiopathy(TMA).
Conclusion
Long-term complement inhibition with eculizumab, with selective transition to ravulizumab, is safe and effective in kidney transplant recipients with aHUS. Graft loss was attributable to rejection rather than aHUS recurrence. Transition to ravulizumab was well tolerated across diverse genetic backgrounds, offering reduced infusion burden without loss of efficacy. Concurrent immunologic challenges including DSA, rejection, and de novo glomerulopathies remain key threats to long-term graft survival.