Abstract: SA-PO0753
Silent Inflammation with Irreversible Damage: A Patient with AA Amyloidosis Presenting with Rapid-Onset Nephrotic-Range Proteinuria
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
- Ghafoor, Elias Alejandro, MedStar Georgetown University Hospital, Washington, District of Columbia, United States
- Pourafshar, Negiin, MedStar Georgetown University Hospital, Washington, District of Columbia, United States
- Kwon, Donghyang, MedStar Georgetown University Hospital, Washington, District of Columbia, United States
Introduction
The widespread use of biologic therapies for chronic inflammatory disorders has widely reduced the incidence of AA Amyloidosis. Nevertheless, delayed recognition continues to occur, particularly in patients with multiple chronic inflammatory and infectious comorbidities. We present a case of rapid-onset proteinuric kidney injury ultimately diagnosed as AA Amyloidosis.
Case Description
A 66M with a history of CKD 3a, HIV, Type 2 Diabetes Mellitus, Polysubstance Use disorder, and Chronic Hepatitis C was brought in by ambulance after being found unresponsive at a bus stop. On admission, he was noted to have a non-oliguric AKI/CKD with a serum creatinine of 2.56 mg/dl. By hospital day 11, serum creatinine had worsened to 3.27 mg/dl. Urinalysis demonstrated proteinuria with spot urine albumin to cr 6.5 g/g and the spot urine protein to cr 17 g/g; serum albumin was low, though, he was normotensive and not anasarcic. All further immunologic and serologic work up was unremarkable. Serum protein electrophoresis revealed polyclonal gammopathy while serum free Kappa/Lambda ratio remained within normal limits at 1.45.
Kidney biopsy demonstrated acellular amorphous deposits on light microscopy. Electron microscopy revealed mesangial proliferation with fibrillary deposition involving both mesangial and interstitial compartments. Notably, congo red staining was positive, confirming amyloid deposition.
Amyloid protein subtype analysis was subsequently sent which revealed AA amyloid subtype.
Discussion
AA Amyloidosis remains an important diagnostic consideration in patients with chronic inflammatory states who develop rapidly progressive proteinuria. This case demonstrates how chronic, clinically silent inflammation can lead to rapid progression from stable CKD to nephrotic range proteinuria and worsening kidney function.
AA Amyloidosis results from prolonged elevation of serum amyloid A, leading to progressive fibril deposition and irreversible organ damage. Early diagnosis is essential as treatment focuses on suppressing the underlying inflammatory process and reducing ongoing amyloid deposition.
This case also highlights the importance of maintaining suspicion for AA amyloidosis in patients with chronic inflammatory or infectious conditions who rapidly develop progressive proteinuria or decline in kidney function, even in the absence of overt systemic inflammation.