Daily urinary interleukin-11 excretion correlated with proteinuria in IgA nephropathy and lupus nephritis

被引:20
作者
Chien, JW
Chen, WL
Tsui, YG
Lee, MC
Lin, AY
Lin, CY
机构
[1] Changhua Christian Hosp, Childrens Hosp, Dept Pediat, Changhua 500, Taiwan
[2] Natl Yang Ming Univ, Inst Med Res, Taipei 112, Taiwan
[3] Chang Jung Christian Univ, Inst Med Res, Coll Hlth Sci, Tainan, Taiwan
[4] Buddhist Tzu Chi Gen Hosp, Dept Pediat, Hualien, Taiwan
关键词
idiopathic nephrotic syndrome; IgA nephropathy; interleukin-11; proteinuria; lupus nephritis; Th1; disease; Th2;
D O I
10.1007/s00467-006-0016-7
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Interleukin-11 (IL-11) is a multifunctional cytokine with both thrombopoietic and anti-inflammatory effects. In an animal study IL-11 was shown to reduce proteinuria in mice with necrotizing glomerulonephritis. The purpose of this current study is to explore the role of IL-11 in human glomerulonephritis. Subjects of this study were patients with proteinuria (daily urine protein excretion > 40 mg/m(2) per hour) and underlying pathology of IgA nephropathy (IgAN) (n=20), lupus nephritis (LN) (n=40), and idiopathic nephrotic syndrome (INS) (n=68). Daily urinary IL-11 level was measured by enzyme-linked immunosorbent assay (ELISA). Correlation between urinary IL-11 and urinary protein was determined by Pearson's correlation coefficient. Another five patients with serial data of urinary protein, IL-11 and IL-11 messenger RNA (mRNA) expression in urine sediment are presented. The correlation between urinary IL-11 and daily urinary protein was significant for patients with IgAN (r=0.596, P=0.006) and LN (r=0.630, P < 0.001), but not for patients with INS (r=0.030, P=0.812). Serial data revealed the same correlation. Furthermore, the peak of urinary IL-11 mRNA preceded that of urinary IL-11. We conclude that daily urinary IL-11 excretion is correlated with urinary protein loss in nephritis having local T helper (Th)1 predominant immune response, such as IgAN and LN. Local IL-11 production may serve as a counter cytokine against Th1-mediated inflammation.
引用
收藏
页码:490 / 496
页数:7
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