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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.
Idiopathic steroid-sensitive nephrotic syndrome (SSNS) is most often encountered in sporadic cases of minimal change disease (MCD) in children. Only rare cases of familial forms of MCD have been reported. The scarcity of familial NS has precluded unraveling the underlying genetic defect and candidate gene approaches have been unsuccessful. We report identical twin sisters with SSNS.
We show clinical data of twin sisters who contemporaneously developed SSNS and review the related literature.
Female monozygotic twins with normal prenatal ultrasound findings, normal amount of amniotic fluid, normal common placenta, and normal female phenotype were born preterm at 33+5 gestational week. Twin A was hospitalized at the age of 4 years due to generalized edema. Laboratory findings showed severe hypoproteinemia (38 g/L) and hypoalbuminemia (14 g/L), severe proteinuria (24-hour urine total protein / creatinine; 3,036 mg / 270 mg), and normal serum creatinine and complement levels. Treatment was started with deflazacort 60 mg/m2/day for 4 weeks followed by tapering and slow reduction. Negative conversion of proteinuria was achieved at two-week of therapy. Two months later, however, dose of steroid was increased because of mild proteinuria, then, tapered successfully. Two months later after the initial onset of nephrotic syndrome in twin A, twin B was admitted due to generalized edema. Laboratory findings showed hypoproteinemia (54 g/L) and hypoalbuminemia (31 g/L), severe proteinuria (24-hour urine total protein / creatinine; 3,668 mg / 310 mg), and normal serum creatinine and complement levels. We treated her with deflazacort as twin A, and in tapering. Negative conversion of her proteinuria was achieved at 8-day of therapy. During ten years twin A and twin B had shown frequent and infrequent relapsing steroid-sensitive features, respectively. Thereafter, both have shown infrequent relapsing steroid-sensitive features, recently.
The identical twins possessed the identical HLA antigens; HLA-A24,33, HLA-B44.5, HLA-C07,14, and HLA-DRB1 07,14. In genetic studies targeted for podocyte molecules, such as, NPHS1, NPHS2, PLCE1, ACTN4, CD2AP, WT-1, TRPC6, LAMB2, were all negative.
We reports a pair of identical female twins who contemporaneously developed idiopathic SSNS. We found that they showed familial feature, however, genetic defects of podocyte molecules were not detected yet.
