Abstract: SA-PO0693
C3 Glomerulonephritis After Candida parapsilosis Lung Infection
Session Information
- Glomerular Diseases: Complement-Mediated Glomerulopathies and Infection-Related GN
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
- Lafond, Alexandre, Pennsylvania Hospital, Philadelphia, Pennsylvania, United States
- Memar, Shadi, Pennsylvania Hospital, Philadelphia, Pennsylvania, United States
- Alborzi, Pooneh, Pennsylvania Hospital, Philadelphia, Pennsylvania, United States
Introduction
C3 glomerulonephritis (C3GN) is a rare disease defined by C3 deposition on immunofluorescence without significant immunoglobulin staining which causes dysregulation of the alternative complement pathway and resultant renal impairment. Common triggers include infectious, autoimmune, and monoclonal gammopathies. Distinguishing C3GN from post-infectious glomerulonephritis (PIGN) is clinically essential, as PIGN is typically self-limited, and C3GN can require immunosuppression or complement-targeted therapy. We present a unique case of C3GN triggered by Candida parapsilosis infection in an immunosuppressed patient.
Case Description
A 75-year-old male with bullous pemphigoid and psoriasis on mycophenolate mofetil (MMF) presented with weight loss, night sweats, fevers, dark urine, and acute kidney injury (Creatinine 2.52 from baseline 0.76 mg/dL). Urinalysis revealed nephrotic-range proteinuria, hematuria, and pyuria. Initial infectious and rheumatologic workup was negative. Complement studies demonstrated low C3, normal C4, elevated Ba and C5, low properdin, abolished alternative pathway activity, and a CFH gene variant of unknown significance. Kidney biopsy showed proliferative glomerulonephritis with dominant C3 staining, sub-endothelial and mesangial deposits, and focal granulomatous inflammation with necrosis, all consistent with C3GN. Despite steroid initiation, renal function declined, requiring hemodialysis. Eculizumab was initiated with quick improvement in urine output. At this time, an addendum was made to the initial kidney biopsy reading, noting necrotizing granulomas. This prompted further infectious workup with CT chest showing diffuse right-sided nodular opacities, and lung biopsy growing rare Candida parapsilosis. Eculizumab was discontinued, and fluconazole was initiated which led to renal recovery and discontinuation of dialysis.
Discussion
To our knowledge, this case represents the first reported association between Candida parapsilosis and C3GN, illustrating the spectrum between PIGN and C3GN in which infections can unmask underlying alternative complement pathway dysregulation. The presence of CFH variant and abolished alternative pathway activity suggests a genetic predisposition triggered by fungal infection in this case.