18 August 2026
: Case report
[In Press] When Infection Mimics Vasculitis: Hydralazine-Induced ANCA-Associated Crescentic Glomerulonephritis in the Setting of Active Infective Endocarditis
Challenging differential diagnosis, Unusual or unexpected effect of treatment, Adverse events of drug therapy, Educational Purpose (only if useful for a systematic review or synthesis), Rare coexistence of disease or pathology
Mohmmed Saleh1ABDEF, Shahrzad Zavoshi1ABDF, Paul Fozo1ADFDOI: 10.12659/AJCR.954110
Am J Case Rep In Press; DOI: 10.12659/AJCR.954110
Available online: 2026-08-18, In Press, Corrected Proof
Publication in the "In-Press" formula aims at speeding up the public availability of the pending manuscript while waiting for the final publication. The assigned DOI number is active and citable. The availability of the article in the Medline, PubMed and PMC databases as well as Web of Science will be obtained after the final publication according to the journal schedule
Abstract
BACKGROUND
Hydralazine-induced antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis is a rare cause of pauci-immune crescentic glomerulonephritis that can closely mimic infection-related renal disease, particularly in the setting of active infective endocarditis. Distinguishing between infection-related glomerulonephritis and drug-induced ANCA-associated vasculitis is clinically important because management strategies differ substantially. We present a case supporting the hypothesis that persistent renal dysfunction despite microbiologic control of infective endocarditis, together with pauci-immune biopsy findings and chronic hydralazine exposure, should prompt consideration of hydralazine-induced ANCA-associated vasculitis rather than infection-related glomerulonephritis.
CASE REPORT
We report the case of a 58-year-old man with a history of bicuspid aortic valve who presented with fatigue, anemia, and acute kidney injury. Blood cultures grew Streptococcus mutans, and echocardiography demonstrated aortic valve vegetations consistent with subacute infective endocarditis. Laboratory evaluation revealed hypocomplementemia, proteinuria, hematuria, and elevated MPO and PR3 ANCA titers. Despite appropriate antimicrobial therapy and clearance of bacteremia, renal dysfunction persisted. Renal biopsy demonstrated pauci-immune crescentic glomerulonephritis consistent with ANCA-associated vasculitis. Further review of the patient’s medications revealed long-term hydralazine therapy, raising concern for hydralazine-induced ANCA-associated vasculitis. Hydralazine was discontinued, and the patient was initiated on high-dose corticosteroid therapy with plans for additional immunosuppressive therapy following recovery from cardiac surgery. The patient subsequently underwent successful bioprosthetic aortic valve replacement with gradual stabilization of renal function.
CONCLUSIONS
This case highlights the diagnostic overlap between infective endocarditis-associated glomerulonephritis and hydralazine-induced ANCA-associated vasculitis. In patients with infective endocarditis who develop persistent renal dysfunction despite appropriate antimicrobial therapy, particularly in the setting of ANCA positivity and chronic hydralazine use, renal biopsy and medication review are essential to establish the correct diagnosis and guide appropriate management.
Keywords: Vasculitis; Endocarditis; Hydralazine; Glomerulonephritis
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