Abstract: TH-PO1109
A Diagnostic Pitfall: Bladder AL Amyloidosis Mimicking Eosinophilic Cystitis
Session Information
- Pathology and Lab Medicine
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Pathology and Lab Medicine
- 1700 Pathology and Lab Medicine
Authors
- Cao, Wenya, The Third Hospital of Xi'an, Xi'an, Shaanxi, China
- Gao, Yi, The Third Hospital of Xi'an, Xi'an, Shaanxi, China
Introduction
Bladder involvement in systemic AL amyloidosis is rare and may mimic inflammatory bladder disease. We report a diagnostically challenging case initially suggestive of eosinophilic cystitis due to marked eosinophilic infiltration.
Case Description
A 54-year-old man with systemic AL amyloidosis presented with recurrent gross hematuria and worsening anemia. Eleven years earlier, renal biopsy confirmed amyloid nephropathy. He had previously received cyclophosphamide-, thalidomide-, and dexamethasone-based therapy but was lost to follow-up.
In April 2025, reevaluation revealed relapsed AL amyloidosis with renal and cardiac involvement, including hypoalbuminemia, elevated NT-proBNP, lambda-predominant free light chains, and IgA-lambda monoclonal gammopathy. Bortezomib plus dexamethasone achieved very good partial hematologic response (VGPR).
Despite hematologic improvement, persistent painless gross hematuria developed after the third cycle. Hemoglobin fell to 80 g/L, and nephrotic-range proteinuria persisted (5.8 g/day). CT urography showed irregular bladder wall thickening; cystoscopy revealed multiple friable lesions. Histology demonstrated stromal edema, reactive urothelial hyperplasia with Brunn nests, and dense eosinophilic infiltration, initially suggesting eosinophilic cystitis. Given his amyloidosis history, Congo red staining and immunofluorescence were performed, confirming AL-lambda amyloid deposition.
The patient underwent transurethral resection and continued plasma cell-directed therapy, with gradual resolution of hematuria.
Discussion
Eosinophilic inflammation can obscure amyloid deposition, mimicking eosinophilic cystitis on routine histology. Amyloid-related vascular injury and chronic inflammation may recruit eosinophils, masking underlying disease unless Congo red staining is performed. Clinically significant bladder involvement occurred despite VGPR, highlighting that hematologic response may not fully reflect tissue-level disease activity and emphasizing the need for ongoing organ-based surveillance.