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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
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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.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Minimal change disease (MCD) is characterized by nephrotic-range proteinuria and hypoalbuminemia. Despite diffuse podocyte foot process effacement on electron microscopy (EM), immune complex deposition is typically absent. By contrast, IgA nephropathy (IgAN) usually presents with hematuria and mild proteinuria but can occasionally cause nephrotic-range proteinuria. Histologically, deposition of IgA and C3 on immunofluorescence staining (IF) is a hallmark of IgAN. We encountered a patient with nephrotic syndrome (NS) whose renal biopsy demonstrated IgA deposition, making the diagnosis challenging.
A 67-year-old male presented with severe edema in lower extremities two months ago. Laboratory tests revealed serum albumin of 2.2 g/dL and urine protein/creatinine ratio of 8.90 g/gCr accompanied with microscopic hematuria, meanwhile renal function remained normal (sCr : 0.83 mg/dL). Renal biopsy showed no glomerular abnormalities in Periodic acid–Schiff and Periodic acid–methenamine silver staining. However, IF staining revealed positivity for IgA and C3 in mesangial area. Furthermore, electron dense deposits in para-mesangial area and partial foot process effacement were observed in EM, establishing the diagnosis with IgA-N.
Steroid pulse therapy (methylprednisolone 500 mg per day for 3 days) was initiated, followed by oral glucocorticoid (GC) given every other day at 30 mg. However, renal dysfunction worsened (sCr : 6.94), necessitating hemodialysis for approximately two weeks. One month later, kidney function was recovered and complete remission (CR) was achieved by GC administrated every other day at 30 mg. Five months later, while tapering GC to 15 mg, NS relapsed with no microscopic hematuria. Low value of selectivity index, recurrence of NS, and histological findings, including foot process effacement led us to consider that MCD, rather than IgA-N, might be a predominant pathology in this case. Thus, steroid pulse therapy and subsequent oral GC at 40 mg per day were started, which immediately resulted in CR.
Although renal biopsy revealed IgA deposition, the rapid development of severe edema, nephrotic-range proteinuria, low value of selectivity index, and prompt responsiveness to immunosuppressants suggested MCD rather than IgA-N as the predominant pathology. The absence of a history of tonsillitis, macrohematuria, and purpura further supported this diagnosis. It remains unclear whether this unusual case of concomitant IgA-N and MCD is a variant form of IgA-N or coincidental IgA deposition in a patient with MCD. However, high-dose GC therapy is deemed necessary according to the standard approach for MCD.
