ArticleKidney & blood pressure research2026
Infective Endocarditis-Associated Glomerulonephritis Caused by
Article in Kidney & blood pressure research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionInfective endocarditis (IE) can trigger systemic embolic and immune-mediated complications, including infection-related glomerulonephritis. When the infectious focus is IE, the condition is termed IE-associated glomerulonephritis (IEAGN). A major diagnostic pitfall is that IEAGN may present with purpura, nephritic urinary abnormalities, systemic inflammation, and antineutrophil cytoplasmic antibody (ANCA) positivity, closely mimicking primary small-vessel vasculitis and risking inappropriate immunosuppression if infection is not promptly excluded. CASE PRESENTATION: A 52-year-old woman with mitral valve prolapse presented with fever, malaise, and palpable purpura. Laboratory testing demonstrated systemic inflammation, renal dysfunction with proteinuria and hematuria, and marked proteinase 3-antineutrophil cytoplasmic antibody (PR3-ANCA) positivity (121 U/mL). Blood cultures obtained for persistent fever yielded Streptococcus cristatus. Transesophageal echocardiography demonstrated large vegetations on the mitral valve (19 mm on the anterior leaflet and 11 mm on the posterior leaflet), with severe mitral regurgitation. Neuroimaging identified a right occipital hemorrhage and small peripheral intracranial aneurysms. Kidney biopsy demonstrated necrotizing and crescentic glomerulonephritis with a granular immune-complex staining pattern on immunofluorescence (C3/C1q/IgG/IgM/IgA) and mesangial electron-dense deposits on electron microscopy, supporting an immune-complex-mediated glomerulonephritis in the setting of IE. She was treated with ceftriaxone and underwent early mitral valve replacement for large vegetations, severe mitral regurgitation, and disseminated lesions. Renal function improved without corticosteroids or other immunosuppressants. During more than 8 weeks of antibiotic therapy, her serum PR3-ANCA level decreased from 121 to 63.8 U/mL by hospital day 73.
conclusionS. cristatus IE can present with vasculitis-like features and a markedly elevated serum PR3-ANCA concentration, closely mimicking ANCA-associated vasculitis. This case emphasizes that ANCA positivity does not rule out infection and highlights the importance of early integration of blood cultures, echocardiography, and renal pathology to support clinicopathological diagnosis and avoid premature immunosuppression.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.