Pathogenesis of Henoch-Schonlein purpura nephritis

被引：107
|
作者：
Lau, Keith K. [1 ]
Suzuki, Hitoshi [2 ,3 ]
Novak, Jan [2 ]
Wyatt, Robert J. [4 ,5 ]
机构：
[1] McMaster Univ, Dept Pediat, Hamilton, ON L8S 3Z5, Canada
[2] Univ Alabama Birmingham, Dept Microbiol, Birmingham, AL 35294 USA
[3] Juntendo Univ, Sch Med, Dept Nephrol, Tokyo 113, Japan
[4] Lebonheur Childrens Hosp & Med Ctr, Childrens Fdn Res Ctr, Memphis, TN USA
[5] Univ Tennessee, Hlth Sci Ctr, Div Pediat Nephrol, Memphis, TN USA
来源：
PEDIATRIC NEPHROLOGY | 2010年 / 25卷 / 01期
关键词：
Henoch-Schonlein purpura nephritis; Children; Galactose-deficient IgA1; Pathogenesis; Immune complex; IGA1-CONTAINING IMMUNE-COMPLEXES; RESONANCE MASS-SPECTROMETRY; PRIMARY IGA NEPHROPATHY; HUMAN MESANGIAL CELLS; HUMAN SERUM IGA1; O-GLYCOSYLATION; COMPLEMENT ACTIVATION; HINGE REGION; GALACTOSYLTRANSFERASE ACTIVITY; GLOMERULAR DEPOSITION;
D O I：
10.1007/s00467-009-1230-x
中图分类号：
R72 [儿科学];
学科分类号：
100202 ;
摘要：
The severity of renal involvement is the major factor determining the long-term outcome of children with Henoch-Schonlein purpura (HSP) nephritis (HSPN). Approximately 40% children with HSP develop nephritis, usually within 4 to 6 weeks after the initial onset of the typical purpuric rashes. Although the pathogenetic mechanisms are still not fully delineated, several studies suggest that galactose-deficient IgA1 (Gd-IgA1) is recognized by anti-glycan antibodies, leading to the formation of the circulating immune complexes and their mesangial deposition that induce renal injury in HSPN.
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页码：19 / 26
页数：8
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