Abstract: SA-PO843
A Rare Case of Renal AA Amyloidosis Secondary to Infectious Etiology
Session Information
- C3G, TMA, MGRS, Amyloidosis, and More
October 26, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Madera, Irvianny, SBH Health System, Bronx, New York, United States
- Jimenez Perez, Lorgis Ignacio, SBH Health System, Bronx, New York, United States
- Flores Chang, Bessy Suyin, SBH Health System, Bronx, New York, United States
Introduction
AA amyloidosis, characterized by the deposition of serum protein amyloid AA, typically arises in inflammatory settings, such as active infections. While renal involvement is common, cases directly linked to pneumonia leading to end-stage renal disease (ESRD) are exceedingly rare. Here, we present such a case, shedding light on its clinical course and management challenges.
Case Description
62-year-old male with history of HIV presented to the hospital due to worsening diarrhea and shortness of breath. On admission, he presented with serum creatinine of 9.2 mg/dL (0.6-1.2 mg/dL) (baseline 0.9 mg/dL, two months prior) and a protein/creatinine ratio of 10. He was found to have cavitary lesions in a Computerized Tomography (CT) scan suggesting unresolved necrotizing pneumonia when compared to previous imaging. In the meantime, he required hemodialysis. Due to nephrotic range proteinuria of unknown etiology, a kidney biopsy was performed which showed severe AA amyloidosis with moderate tubular atrophy and interstitial fibrosis. Unfortunately, the patient remains in hemodialysis.
Discussion
We describe a patient with a rapid decline in renal function for whom we hypothesize that the ongoing infection in his immunosuppressive state led to reactive AA amyloidosis. Renal AA amyloidosis is presented rarely in adult-age patients. One case is described similar to our patient where renal AA amyloidosis was caused by pulmonary Mycobacterial infection associated with diarrhea. However, in our patient, none of the acid-fast bacilli cultures were positive. The standpoint in management is decreasing the inflammatory environment in the patient, however since our patient already had moderate tubular atrophy, prognosis remained poor.
Kidney histology showing AA amyloidosis in H&E stain (left) and immunohistochemistry (right).