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Macrophage inflammatory protein‐1β and interleukin‐8 associated with idiopathic steroid‐sensitive nephrotic syndrome
Author(s) -
Kanai Takahiro,
Yamagata Takanori,
Momoi Mariko Y.
Publication year - 2009
Publication title -
pediatrics international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.49
H-Index - 63
eISSN - 1442-200X
pISSN - 1328-8067
DOI - 10.1111/j.1442-200x.2008.02759.x
Subject(s) - medicine , nephrotic syndrome , cytokine , group b , immunology , population , group a , interleukin , gastroenterology , environmental health
Abstract Background: The cytokines associated with idiopathic steroid‐sensitive nephrotic syndrome (ISSNS) have not been identified definitively, because previous studies had variable sampling and population heterogeneity. To clarify the cytokines involved, serum cytokine levels were measured using uniform sampling in a homogeneous population. Methods: Five children meeting the following criteria were included: (i) ISSNS; (ii) selectivity index <0.1; (iii) paired sera obtained in the nephrotic phase before steroid treatment (STx; group A) and in the remission phase under STx (group B); (iv) no infection; and (v) no immunosuppressant. Control groups were as follows: group C, four children with ISSNS in the remission phase without STx; group D, five with normal urinalysis; group E, five with symptomatic secondary nephrotic syndrome before STx. Cytokine levels were measured using bead‐based assay. Results: Serum macrophage inflammatory protein‐1β (MIP‐1β) levels were higher in group B compared to group A, and group C was lower than groups A and B. Serum interleukin‐8 (IL‐8) levels were higher in group A than in groups B and C, and groups B and C did not differ. With regard to both cytokine levels, there were no differences between groups C and D, and groups A and E. Conclusion: Serum MIP‐1β and IL‐8 are associated with the clinical status of ISSNS in children. A relationship between MIP‐1β and ISSNS has not been previously reported. The mechanism by which MIP‐1β and IL‐8 affect ISSNS is unclear. Nevertheless, the present findings are an interesting starting point for further investigations into the pathophysiology of ISSNS in children.