期刊
KIDNEY INTERNATIONAL
卷 75, 期 12, 页码 1330-1339出版社
ELSEVIER SCIENCE INC
DOI: 10.1038/ki.2009.71
关键词
cytokines; galactose deficiency; human mesangial cells; IgA nephropathy; macromolecular IgA1; multiplex IgAN family
资金
- Research Grant Committee (Hong Kong) [HKU 7697/07M]
- L & T Charitable Foundation
- House of INDOCAFE
Multiple cases of IgA nephropathy (IgAN) may occur in families; we compared their prognosis to sporadic cases of this disease. We isolated macromolecular IgA1 from 60 patients with familial IgAN, 91 of their asymptomatic relatives, 43 patients with sporadic IgAN (SpIgAN), 90 of their asymptomatic relatives, and 43 healthy subjects. Compared with SpIgAN patients, those with multiplex familial IgAN (MpIgAN) had more advanced renal histopathology and more galactose-deficient macromolecular IgA1 in their serum. Further, when we tested the effects of the macromolecular IgA1 on human mesangial cells in culture, we found that the macromolecular IgA1 taken from familial clusters had enhanced binding to mesangial cells and caused increased expression of interleukin-6, tumor necrosis factor-a, and monocyte chemotactic peptide-1. The macromolecular IgA1 isolated from asymptomatic relatives caused increased cytokine expression in the mesangial cells when derived from MpIgAN compared with SpIgAN or healthy controls. While these studies suggest that macromolecular IgA1 isolated from patients with MpIgAN is more pathogenic than that from patients with SpIgAN, long term follow-up will be needed to clarify the risk in asymptomatic relatives of the patients with multiplex familial disease. Kidney International (2009) 75, 1330-1339; doi:10.1038/ki.2009.71; published online 1 April 2009
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