SERUM AND URINE SOLUBLE INTERLEUKIN-2 RECEPTOR IN IDIOPATHIC NEPHROTIC SYNDROME

被引:29
|
作者
BOCK, GH
ONGKINGCO, JR
PATTERSON, LT
RULEY, J
SCHROEPFER, LR
NELSON, DL
机构
[1] Immunophysiology Section, Metabolism Branch, DCBDC, National Cancer Institute, Bethesda, Maryland
[2] Department of Nephrology, Children's National Medical Center, Washington, District of Columbia, 20010
[3] Department of Pediatrics, George Washington University School of Medicine, Washington, District of Columbia
[4] Howard Hughes Medical Institute-National Institutes of Health Research Scholars Program, Bethesda, Maryland
关键词
MINIMAL CHANGE NEPHROTIC SYNDROME; PATHOGENESIS; INTERLEUKIN-2; RECEPTOR; URINE AND SERUM;
D O I
10.1007/BF00852533
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Although a cellular immune pathogenesis is suspected in idiopathic nephrotic syndrome of childhood (INS), there is scant direct evidence of in vivo immune activation. In order to investigate cytokine cascade activation in INS, soluble interleukin-2 receptor (sIL-2R) in plasma and urine was characterized and its levels measured in INS patients during relapse. Immunochemically detectable sIL-2R had a molecular mass of 35-46 kDa in both serum and urine and the molecule appears to be excreted intact; the pI was 5.05. INS patients had elevated serum sIL-2R levels compared with adult normal controls (845 +/- 97 vs. 373 +/- 47 U/ml, P = 0.001) and were significantly higher than previously published age-matched controls. Urinary excretion of sIL-2R was 47.2 +/- 13 U/mg creatinine in patients. Both the sIL-2R excretion rate and the fractional excretion of sIL-2R were positively correlated with the excretion of albumin (P = 0.02 and 0.002, respectively). These increased serum and urine levels occurred whether relapse was or was not associated with an intercurrent illness. We conclude that: (1) despite increased sIL-2R excretion during INS relapse, serum levels are significantly elevated; (2) while the elevated urinary levels could result from enhanced intrarenal production, they more likely reflect the increased serum levels; (3) the elevated sIL-2R levels support an immune pathogenesis in INS.
引用
收藏
页码:523 / 528
页数:6
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