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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.
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Abstract titles should be brief and reflect the content of the abstract.
While cirrhosis-associated IgA nephropathy has been well documented, systemic IgA vasculitis (IgAV) developing in this context is extremely uncommon. Among the various etiologies of cirrhosis, metabolic dysfunction–associated steatohepatitis (MASH) represents a distinct metabolic phenotype induced by chronic inflammation, and only a few IgA-related kidney or vasculitic diseases have been described in this setting. We report a rare case of biopsy-proven IgAV occurring in a patient with MASH-related cirrhosis, resulting in hepatic decompensation after corticosteroid therapy.
A 78-year-old woman with type 2 diabetes and compensated MASH-related cirrhosis (Child–Pugh score 6) presented with recurrent fever, palpable purpura, and intermittent gross hematuria.Urinalysis showed glomerular hematuria and proteinuria (1.57 g/gCr). Serum IgA was markedly elevated (985 mg/dL) with normal complement and low C-reactive protein (0.42 mg/dL).Serum albumin was 2.8 g/dL, consistent with underlying hepatic dysfunction. Skin biopsy demonstrated leukocytoclastic vasculitis, and renal biopsy revealed ISKDC class IIIa IgAV with one cellular crescent.She received half-pulse methylprednisolone followed by oral prednisolone (30 mg/day). Marked hyperglycemia appeared soon after corticosteroid initiation, and after four weeks, progressive leg edema and tense ascites developed, with worsening Child–Pugh score (6→8).She was readmitted and treated with albumin infusion, intensified diuretics (loop diuretic plus mineralocorticoid receptor antagonist), and reduction of prednisolone to 20 mg/day.Her ascites and edema gradually improved thereafter.
In cirrhosis, impaired hepatic clearance of IgA immune complexes and portosystemic shunting can result in their persistence within the systemic circulation.Abnormal IgA production may further contribute to the accumulation of aberrantly glycosylated IgA, which most often presents clinically as IgA nephropathy.In MASH-related cirrhosis, chronic metabolic inflammation induced by insulin resistance and lipotoxicity may amplify IgA production and alter its glycosylation pattern, possibly creating a systemic environment prone to IgA-mediated immune injury.Corticosteroid therapy, although effective in controlling vasculitic inflammation, can exacerbate metabolic dysfunction through worsening insulin resistance and sodium retention.In patients with MASH-related cirrhosis, these effects may further disturb hepatic homeostasis, predisposing to fluid overload and hepatic decompensation.
This case highlights the potential link between metabolic liver disease and systemic IgAV, suggesting that corticosteroids should be used with caution in patients with impaired hepatic and metabolic reserve.
