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.
Adult-onset Still's disease (AOSD) is a rare systemic inflammatory disease and renal involvement is relatively uncommon. We report a case of AOSD presenting with rapidly progressive glomerulonephritis (RPGN) and complicated by AA amyloidosis, which was successfully treated with Tocilizumab.
A 50-year-old woman. Thirteen years ago, she presented with fever, urticaria-like erythema, and generalized lymphadenopathy, leading to a diagnosis of AOSD. She was treated with prednisolone (PSL). During the course of the disease, she experienced multiple exacerbations, each treated with immunosuppressive therapy. In X year, lower limb edema developed. Blood tests revealed rapid deterioration of renal function (Cr 0.86→1.6 mg/dL) along with proteinuria and hematuria. At admission, blood tests showed TP/Alb(g/dL): 6.5/3.2, CRP: 13.76 mg/dL, BUN: 42 mg/dL, Cre: 1.73 mg/dL, eGFR: 25.1 mL/min/1.73 m², and urinary protein/creatinine Ratio: 3.43 g/gCr, respectively. Renal biopsy showed amorphous deposits in mesangium area, glomerular tuft, vessel walls of the interlobular arteries and afferent arterioles. Positive DFS staining and amyloid A staining led to a diagnosis of AA amyloidosis. In addition to that, cellular crescents were observed in 20% of glomeruli. The dose of PSL was increased to 30 mg and additionally steroid pulse therapy was undergone, even though CRP remained elevated. Therefore, tocilizumab therapy was initiated. Following tocilizumab administration, serum CRP concentration decreased to within the normal range, and urinary protein/creatinine Ratio decreased to 0.28 g/gCr. Serum amyloid A (SAA) decreased from A to B.
Renal complications associated with AOSD include AA amyloidosis, IgA nephropathy, and collapsing glomerulopathy; however, cases of AA amyloidosis complicated by crescent formation are extremely rare. In the present case, amyloid deposition along glomerular tufts and the rupture of glomerular GBM at the site of amyloid deposition were identified, suggesting that amyloid deposition caused the rupture of GBM, resulting in glomerular crescent formation and rapid decline in kidney function. SAA is an acute phase apolipoprotein reactant produced primarily by hepatocytes under the control of proinflammatory cytokines including interleukin (IL)-6, and some previous studies indicate that IL-6 is the main pathological player to produce SAA. Thus, tocilizumab, IL-6-specific inhibitor, might have played important role in reducing proteinuria, maintaining kidney function, and suppressing long-term systemic inflammation in AOSD.
Tocilizumab prevented the progression of AA amyloidosis derived from adult-onset still disease.
