Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Infection-related glomerulonephritis (IRGN) can present atypically with C3-dominant deposits and features overlapping C3 glomerulopathy (C3G), lacking the classic subepithelial 'humps' of post-streptococcal glomerulonephritis (PSGN). Because the clinical and pathological findings are often similar, differentiating these two conditions presents a significant diagnostic challenge, particularly in severe adult-onset cases.
A 55-year-old man was referred to our hospital for marked hypertension, systemic edema and rapidly progressive glomerulonephritis (RPGN) that began two weeks prior. On presentation, laboratory findings showed acute kidney injury (creatinine 3.15 mg/dL, eGFR 17.6 mL/min/1.73m²), nephrotic-range proteinuria (UPCR 12.42 g/gCr), and hypoalbuminemia (2.8 g/dL). Serology was notable for a high anti-streptolysin O (ASO) titer (1107 IU/mL) and an isolated decrease in serum C3 (35 mg/dL), with normal C4 (41 mg/dL). He complained of chronic pharyngeal discomfort, but the rapid antigen test for streptococcal was negative. Serological autoantibodies, including ANCA and anti-GBM antibodies, were negative. A kidney biopsy demonstrated a diffuse endocapillary proliferative and crescentic glomerulonephritis in 7 of 35 glomeruli. Immunofluorescence demonstrated C3-dominant (3+) granular deposits in the mesangium and capillary, with weaker staining for IgG(1+) and IgA(+) in the mesangium. Electron microscopy confirmed abundant mesangial and subendothelial dense deposits but, critically, lacked prominent subepithelial 'humps'. Furthermore, no organized structures or intramembranous dense deposits were observed. Subsequent immunostaining for nephritis-associated plasmin receptor (NAPlr) was positive in glomeruli. Although his serum complement levels normalized spontaneously, kidney function and severe proteinuria did not improve. Therefore, steroid therapy (prednisone 30 mg/day) was started at week 12. By week 21, his creatinine improved to 2.49 mg/dL, and proteinuria dramatically decreased to 0.63 g/gCr. This case of a NAPlr-positive, crescentic glomerulonephritis highlights the significant the overlap between atypical IRGN and C3G. Our findings suggest that IRGN should be considered in the differential diagnosis in adult-onset crescentic glomerulonephritis with a C3-dominant profile, even in the absence of classic pathological features.
