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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.
Psoriasis is a common chronic immune-mediated disease that causes not only papulosquamous skin lesions but also affects various organs. Overactivation of adaptive immune cells, especially helper T cells (Th1 and Th17), plays an important role in the pathogenesis of psoriasis. We report an elderly patient whose drug allergy–induced psoriasis flare was followed by the development of IgA vasculitis with kidney dysfunction.
An 81-year-old Japanese man with a 19-year history of psoriasis had been receiving topical methylprednisolone ointment. He had a 16-year history of diabetes mellitus and subsequently developed declining kidney function.
He fell at home, resulting in left leg hemorrhage and hypotension (BP 90/50 mmHg), and was transferred to our hospital. On admission, he was found the severe anemia (Hb 6.6 g/dL), received a blood transfusion, and underwent embolization using interventional radiology techniques, after which his vital signs stabilized. However, he subsequently developed pneumonia and was started on antibiotic therapy.
Five days later, the patient developed a rash, and blood tests revealed elevated eosinophil levels. The drug-induced lymphocyte stimulation test (DLST) was positive, suggesting a drug-induced reaction, and the antibiotics were discontinued. The abdominal and back rash gradually improved; however, his psoriasis worsened. He developed progressive psoriasis on the scalp, elbows, and knees, which were more severe than at baseline.
Soon after, the patient developed palpable purpura on the legs, hematuria and decline in kidney function. Laboratory investigations showed elevated levels of C-reactive protein (4.96 mg/dL) and fibrinogen (458 mg/dL). Serum IgA was markedly elevated (592 mg/dL), while IgG and IgM levels remained within normal ranges. Vasculitis was suspected, and we consulted a dermatologist.
Skin biopsy revealed leukocytoclastic vasculitis with C3 and IgA deposition in dermal capillaries. The patient was diagnosed with IgA vasculitis causing renal dysfunction and treated with intravenous methylprednisolone (500 mg/day for three days), followed by continued steroid therapy at a dose of 0.8 mg/kg. The skin lesions improved significantly, but kidney function remained impaired. The prednisolone dose was gradually tapered.
Psoriasis is a T-cell–mediated chronic inflammatory skin condition, in which activated immune cells and cytokines can circulate systemically and affect multiple organs. Drug allergy, a type IV hypersensitivity reaction, may amplify these immune pathways. While psoriasis is primarily recognized as a dermatological disorder, its systemic inflammation can influence other organs, including the kidneys.
In our patient, a drug allergy–induced psoriasis flare was followed by the onset of IgA vasculitis with kidney dysfunction. This temporal relationship suggests that psoriasis exacerbation may not only reflect skin involvement but also trigger abnormal IgA immune responses that contribute to renal injury. This case emphasizes the importance for nephrologists to consider psoriasis flares as potential triggers of IgA-mediated kidney disease.
