Abstract: FR-PO0768
A Silent Heart, a Broken Kidney: The Diagnostic Challenge of Infective Endocarditis-Associated Rapidly Progressive Glomerulonephritis
Session Information
- Glomerular Diseases: ANCA Vasculitis, Anti-GBM Disease, and Crescentic GN
October 23, 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
- Khurana, Shriya, MedStar Washington Hospital Center, Washington, District of Columbia, United States
- Thach, Lonnie, MedStar Washington Hospital Center, Washington, District of Columbia, United States
Introduction
Rapidly progressive glomerulonephritis (RPGN) is classically associated with ANCA-associated vasculitis or anti–glomerular basement membrane disease, while infective endocarditis (IE) typically causes immune complex–mediated glomerulonephritis. We report a rare case of IE-associated pauci-immune RPGN, highlighting a diagnostic and therapeutic dilemma.
Case Description
A 47-year-old male with diabetes, hypertension and coronary artery disease presented with dyspnea and chest pain. Evaluation revealed severe acute kidney injury (creatinine 9.99 mg/dL from baseline 0.8), anemia, and leukocytosis. Urinalysis showed hematuria, proteinuria, and RBC casts. Serologic workup, including ANA, anti-dsDNA, MPO-ANCA, PR3-ANCA, anti-GBM antibodies, and viral studies, was negative; complements were normal. ANCA by immunofluorescence was low-titer positive (c-ANCA 1:80) without MPO/PR3 specificity. Renal biopsy demonstrated diffuse proliferative glomerulonephritis with rare crescents and negative immunofluorescence, consistent with pauci-immune crescentic glomerulonephritis (Image).
Blood cultures grew Streptococcus mitis. Echocardiography one month prior had shown mitral regurgitation with Lambl’s excrescence but no vegetations. Repeat imaging revealed mitral and aortic valve vegetations with new aortic regurgitation, confirming IE. Immunosuppression was deferred due to active infection. Despite intravenous antibiotics, renal function did not recover, and the patient remained dialysis-dependent until undergoing valve replacement. Postoperatively, renal function improved (creatinine 5.02 to 2.18 mg/dL), allowing reduced dialysis frequency.
Discussion
This case challenges the paradigm that IE-associated glomerulonephritis is uniformly immune complex–mediated by demonstrating a pauci-immune pattern with negative ANCA serologies. It underscores a therapeutic dilemma of immunosuppression in infection-associated crescentic GN. In this case, renal recovery occurred only after definitive surgical source control, highlighting the importance of timely valve intervention in IE-associated RPGN.
Renal Biopsy