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Atopy, serum IgE, and interleukin-13 in steroid-responsive nephrotic syndrome

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Abstract

Earlier studies have demonstrated a strong association of steroid-responsive nephrotic syndrome (SRNS), atopy, and elevated serum IgE levels. Interleukin (IL-13) gene expression is significantly increased in children with SRNS in relapse. As interferon (IFN)-γ, IL-13, and IL-4 have regulatory effects on IgE synthesis, we examined the relationship between intracellular cytokine production and serum IgE levels in children with SRNS, in order to further define the reported association with atopy. The median serum IgE levels in nephrotic patients in relapse with (492 U/ml) or without atopy (561 U/ml) were significantly higher than those in remission (221 U/ml, P<0.002 or 90 U/ml, P<0.001, respectively) and non-atopic controls (177 U/ml) (P<0.001). The percentage of CD3+ IL-13-producing cells was significantly higher in nephrotic children in relapse, and correlated with the serum IgE levels during the active phase of the disease (r=0.90, P<0.001). These data suggest that the elevated serum IgE levels during relapses of SRNS were the result of upregulation of IL-13. This probably reflects some common immune activation following various stimuli, rather than a direct association with atopy.

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Acknowledgements

This work was supported by a grant (NMRC/0083/1995) from the National Medical Research Council, Singapore.

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Authors and Affiliations

  1. Department of Pediatrics, National University of Singapore, 5 Lower Kent Ridge Crescent, 119074, Singapore

    Wai Cheung, Chang-Li Wei, Ching-Ching Seah & Hui-Kim Yap

  2. Steven Spielberg Pediatric Research Center, Cedars-Sinai Medical Center, UCLA School of Medicine, Los Angeles, CA 90028, USA

    Stanley C. Jordan

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  1. Wai Cheung
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  2. Chang-Li Wei
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  3. Ching-Ching Seah
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  4. Stanley C. Jordan
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  5. Hui-Kim Yap
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Correspondence to Hui-Kim Yap.

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Cheung, W., Wei, CL., Seah, CC. et al. Atopy, serum IgE, and interleukin-13 in steroid-responsive nephrotic syndrome. Pediatr Nephrol 19, 627–632 (2004). https://doi.org/10.1007/s00467-004-1438-8

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  • DOI: https://doi.org/10.1007/s00467-004-1438-8

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