Abstract: FR-PO0938
Intravenous Immunoglobulin-Associated Thrombotic Microangiopathy in a Kidney Transplant Recipient
Session Information
- Glomerular Case Reports: Lupus, FSGS, Complement, and More
November 07, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Loon, Jordan, Albany Medical Center, Albany, New York, United States
- Perlmutter, Jason Jessie, Albany Medical Center, Albany, New York, United States
- Pal, Aman, Albany Medical Center, Albany, New York, United States
- Faddoul, Giovanni, Albany Medical Center, Albany, New York, United States
Introduction
Thrombotic microangiopathy (TMA) in a kidney transplant recipient can have multiple potential causes including antibody mediated rejection, infection, and drug toxicity. Our case highlights a case of intravenous immunoglobulin (IVIG)-associated TMA.
Case Description
A 73-year-old woman status post deceased-donor kidney transplant 7 years prior presented with fatigue, oliguria, hyperkalemia with EKG changes, and a creatinine of 10.2mg/dL from a baseline of 2.5 less than a month ago. Immunosuppressive regimen included tacrolimus 0.5mg with belatacept every 8 weeks that was adjusted due to previous recurring infections. She had recently been diagnosed with dermatomyositis based on an MRI finding and was initiated on IVIG therapy the week prior to presentation. She received a total of three doses of 0.75g/kg each, three days in a row. Labs revealed thrombocytopenia and low haptoglobin. She was initiated on CRRT then transitioned to hemodialysis. Kidney biopsy showed acute TMA with arterial intimal inflammation and peritubular capillaritis. Her presentation initially raised concern for TMA secondary to antibody-mediated rejection (AMR). AMR was then deemed unlikely due to lack of C4d staining in the allograft in addition to declining donor-specific antibody levels, and lack of chronic antibody mediated rejection. Osmotic tubular injury typical of calcineurin inhibitor toxicity was additionally not present. The timing of symptom onset within a week of IVIG administration strongly supported a diagnosis of IVIG-associated TMA. She was then treated with eculizumab, resulting in resolution of anemia and thrombocytopenia and gradual improvement in kidney function with decrease in frequency of dialysis 6 weeks from the start of eculizumab.
Discussion
Biopsy findings, exclusion of other etiologies, and favorable response to eculizumab point to IVIG-associated TMA in this case. Rare cases of TMA caused by IVIG therapy have been reported previously. Differentiating between TMA secondary to AMR vs IVIG was crucial in this case as antibody mediated rejection has different therapeutic implication and IVIG itself is often used as treatment in AMR. Prompt recognition of IVIG as a potential trigger for TMA allowed for targeted treatment with complement inhibition. Clinicians should maintain a high index of suspicion when new-onset kidney injury follows recent IVIG administration.