Abstract: SA-PO246
Fungal Endocarditis and ANCA-Vasculitis: More Than a Mere Coincidence?
Session Information
- Trainee Case Reports - V
October 27, 2018 | Location: Exhibit Hall, San Diego Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Reports
- 1203 Glomerular Diseases: Clinical, Outcomes, and Trials
Authors
- Aboud, Hussain, University of Florida, Gainesville, Florida, United States
- Clapp, William L., University of Florida, Gainesville, Florida, United States
- Koratala, Abhilash, University of Florida, Gainesville, Florida, United States
Introduction
Glomerulonephritis (GN) due to infective (bacterial) endocarditis is well documented, with the most common lesions being necrotizing and crescentic GN, followed by endocapillary proliferative GN. Prominent C3 staining and subepithelial immune deposits on EM are commonly associated with infection-related GN than Pauci-immune picture of ANCA vasculitis. Herein, we present a case of Pauci-immune proliferative GN in a patient with fungal endocarditis.
Case Description
A 52-year-old White man with a history of intravenous drug abuse, chronic hepatitis C and diabetes mellitus initially presented to our institution with fever and bilateral lower extremity rash/palpable purpura. Biopsy of the rash demonstrated small and medium vessel vasculitis. He was also found to have native aortic valve endocarditis with ~1.5 cm vegetation and Candida parapsilosis fungemia which failed treatment with Micafungin and therefore switched to amphotericin B and flucytosine. Later, he developed worsening renal function with sub-nephrotic proteinuria and work up revealed dysmorphic RBCs in the urine, hypocomplementemia, positive C-ANCA, PR3 and cryoglobulins. In the presence of multiple confounding factors and varied differentials (e.g. hepatitis C-MPGN, post-infectious GN, ANCA vasculitis), a renal biopsy was obtained which showed proliferative Pauci-immune glomerulonephritis with ATN [Figure]. His renal function worsened requiring dialysis. Immunosuppressive therapy was not attempted because of active fungemia.
Discussion
Interestingly, ANCA antibody is found in up to 28% of the tested patients with infective endocarditis. However, Post-infectious Pauci-immune GN in association with Candida parapsilosis has never been reported in the literature to the best of our knowledge. It is likely that the fungal capsular polysaccharide activates complement cascade and triggers inflammation. Whether ANCA-antibody was a coexistent distinct entity or induced by fungal infection or underlying hepatitis C in our patient remains elusive.