Abstract: SA-PO1188
Immediate Post-Transplant Thrombotic Microangiopathy: A Case Series of Early Onset, Etiologic Differentiation, and Clinical Outcomes
Session Information
- Transplantation: Clinical - Complications, Pediatrics, and Multi-Organ Considerations
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2002 Transplantation: Clinical
Authors
- Bijjala, Neha, University of California San Diego, La Jolla, California, United States
- Macedo, Etienne, University of California San Diego, La Jolla, California, United States
- Shah, Mita, University of California San Diego, La Jolla, California, United States
- Khan, Adnan A., University of California San Diego, La Jolla, California, United States
- Jabbour, Moussa, University of California San Diego, La Jolla, California, United States
Introduction
Thrombotic microangiopathy (TMA) arising within the first days following kidney transplantation is a rare, life-threatening complication driven by endothelial injury and microvascular thrombosis. The immediate post-transplant window is uniquely predisposed to TMA through a mixture of etiologies, including ischemia-reperfusion injury (IRI) and peak calcineurin inhibitor (CNI) exposure. Distinguishing these entities and determining optimal therapy remains challenging.
Case Description
We retrospectively reviewed six renal allograft recipients who developed post transplant TMA at our center. Demographics, donor type, laboratory data, complement and ADAMTS13 activity, donor-specific antibodies (DSA), genetic panel results, treatment, and outcomes were analyzed.
Patients ranged in age from 24–67 years (3M:3F). Underlying ESKD etiologies included FSGS (n=3), HTN nephrosclerosis, tubulointerstitial nephritis, and unknown. Donors were DCD (n=4) and DBD (n=2). TMA onset occurred 1–4 days post-operatively. All patients met hematologic TMA criteria: schistocytes present in 6/6, thrombocytopenia (platelets 5–24), elevated LDH (484–2031), and undetectable haptoglobin (<10) in all. ADAMTS13 activity was preserved in 4/6 (range 63–91%) and mildly reduced in 2/6 (41%), excluding TTP. Elevated soluble C5b-9 was seen in 2/6 (450, 319). DSA was present in 2/6. Genetic panel testing for TMA/aHUS yielded equivocal results (variants of uncertain significance or ADAMTS13 variants) in 4/6. Biopsy was performed in 1/6, confirming concurrent TCMR and AMR. Probable etiologies included IRI (n=1), CNI-induced TMA (n=2), and mixed IRI/CNI (n=2). All patients were switched from tacrolimus to cyclosporine. Therapeutic plasma exchange was used in 4/6 (3–8 sessions). Eculizumab was administered in 5/6 for 3 weeks to 1 year. TMA resolved in all 6 patients.
Discussion
Immediate post-transplant TMA is frequently multifactorial, with IRI and CNI induced TMA as predominant drivers. Equivocal genetic panel results complicate aHUS diagnosis. Early CNI conversion, TPE, and complement inhibition with eculizumab were associated with universal TMA resolution. Prospective data are needed to define optimal eculizumab duration in this population.