Abstract: TH-PO1110
Combined IgAN and AA Amyloidosis: Parallel Renal Consequences of Chronic Infection
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
- Mahoney, Sean P., Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States
- Kapitsinou, Pinelopi P., Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States
- Paparello, James J., Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States
- Ellis, Carla L., Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States
Introduction
IgA nephropathy and SAA amyloidosis are recognized complications of chronic inflammatory disease, though with distinct pathogenic mechanisms and clinical implications. Their simultaneous occurrence at renal biopsy is exceedingly rare and seldom described in literature.
Case Description
Case 1: A 36 year old male presented to the ED with a past medical history of bacterial endocarditis. His creatinine was 0.6 at baseline, but was over 5.0 on presentation. A kidney biopsy showed extensive amyloidosis with near replacement of glomerular structures, IgA dominant mesangial staining and amyloid fibrils involving vessels and glomerular basement membranes with concurrent mesangial electron densities on electron microscopy (EM).
Case 2: A 43 year old female with a history of IVDU presented to the ED with lower extremity edema. Serum creatinine was 3.0 (baseline unknown) with nephrotic range proteinuria. She had MRSA infection of lower extremity wounds. A renal biopsy showed amyloid expanding mesangial areas, IgA dominant mesangial staining and amyloid fibrils involving vessels and glomerular basement membranes with concurrent mesangial electron densities on EM (see figure). Amyloid was typed as SAA on both cases by mass spectrometry.
Discussion
The occurrence of both IgAN and SAA amyloidosis in each case likely reflects convergent pathophysiology driven by bacterial infection and not necessarily a pathogenic relationship between the two diseases, however; we bring attention with these cases to two generally distinct diagnoses that can coincide. Chronic infection triggers sustained pattern recognition of receptor activation, initiating a downstream cytokine cascade centered around IL-6. This drives hepatic serum amyloid A (SAA) and independently dysregulates mucosal IgA O-glycosylation. Therefore, a single infectious process can produce two phenotypically different renal lesions, and it is important to recognize that one diagnosis does not preclude the other. More recognition of these two coinciding diagnoses will hopefully lead to a better understanding of the pathophysiology involved.