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Studies on the Prognostic Marker in Minimal Change Nephrotic Syndrome

Journal of the Korean Pediatric Society 1993;36(7):906-912.
Published online July 15, 1993.
Studies on the Prognostic Marker in Minimal Change Nephrotic Syndrome
Byoung-Soo Cho
Department of Pediatrics, College of Medicine, Kyung Hee University, Seoul, Korea
미세변화 신증후군의 예후표지자에 관한 연구
경희대학교 의과대학 소아과학교실
Childhood minimal change nephrotic syndrome (MCNS) is often associated with hyper-sensitivity reactions and considered to be caused by immune dysfunction. The elevated serum IgE levels and atopic symptoms have been frequently associated in these patients. The present therapy for MCNS mainly depends on corticosteroids, alkylating agents such as chlorambucil, cyclophosphamide and cyclosporin A (Cy-A). Howerver, frequent relapses and severe side effects caused by such therapy necessitate development of a more specific and effective therapeutic regimen. Recently, a T cell derived cytokine, interleukin 4 (IL-4) is being recognized as a major cytokine up-regulating IgE production and response, while interferon-γ (IFN-γ) counteracts IL-4 actions to down-regulate the IL-4 induced IgE response. Hence, the present study is aimed to investigate the role of IL-4 in MCNS. Using freshly isolated peripheral blood from active MCNS patients and normal controls, it was fround that not only serum IgE levels, but also membrane-bound IgE receptor expression and soluble IgE receptor production were also significantly higher in MCNS than in normal controls, which in turn correlated well with the increased IL-4 activities in the patients?sera. Interestingly among MCNS patients receiving a steroid therapy, those who responded with a clinical remission demontrated a noticeable decrease in IgE receptor levels on their B cells. From these results it is concluded that MCNS is highly associated with not only increased serum IgE, but also elevated IL-4 activities and IgE receptor expression. In addition, IgE receptor could be a good prognostic marker in MCNS.
Key Words: Minimal Change Nephrotic syndrome, Interleukin-4, IgE-receptor

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