Abstract: SA-PO0780
Success Treatment of AA Amyloidosis with Tocilizumab
Session Information
- Glomerular Diseases: Lupus Nephritis, Monoclonal Gammopathy-Related Disease, and Transplantation
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Zheng, Sijie, The Permanente Medical Group Inc, Oakland, California, United States
- Jain, Anagha, The Permanente Medical Group Inc, Oakland, California, United States
Introduction
AA amyloidosis is a complication of chronic inflammation driven by sustained inflammatory process. Treatment has been aimed at treating underlying inflammatory conditions. However, when underlying inflammatory process cannot be controlled or identified, there are very limited options. We present a case of AA amyloidosis manifesting as nephrotic syndrome in a patient with clinically controlled rheumatoid arthritis (RA) and inflammatory bowel disease (IBD).
Case Description
A 60 y.o. Hispanic man with clinically stable RA and IBD on Sulfasalazine, presented with sudden onset of AKI with UPCR of 25 mg/mg, edema and serum albumin of 1.5 mg/dl after cholecystectomy. He was taking NSAIDs after surgery for two weeks. Serologic and hematologic workup for autoimmune and paraproteinemic causes was negative. Imaging and infectious evaluation did not identify an inflammatory source. Kidney biopsy demonstrated Congo red–positive deposits with apple-green birefringence, with typing consistent with AA amyloidosis. The patient’s RA was well controlled with no signs or symptoms of inflammation, repeat colonoscopy shown normal colon and terminal ileum. Given concern for occult inflammation, therapy with the interleukin-6 (IL-6) inhibitor Tocilizumab was initiated to suppress serum amyloid A production. The patient had marked clinical improvement, including resolution of edema, UPCR decreased to 5.5 g/g and serum albumin increased to 3.2 mg/dl (Figure).
Discussion
This case highlights that AA amyloidosis can develop despite clinically quiescent inflammatory disease, likely due to ongoing subclinical cytokine activity. IL-6 plays a central role in regulating serum amyloid A synthesis, and its inhibition represents a targeted therapeutic strategy in AA amyloidosis when a clear inflammatory driver is not evident.
Acknowledgment
We gratefully acknowledge the patient for providing consent to share his clinical course and contributing to advancing our understanding of this rare condition.