Complement-mediated kidney diseases

被引:38
作者
Poppelaars, Felix [1 ]
Thurman, Joshua M. [2 ]
机构
[1] Univ Groningen, Univ Med Ctr Groningen, Dept Internal Med, Div Nephrol, AA53,Postbus 196, NL-9700 AD Groningen, Netherlands
[2] Univ Colorado Anschutz Med Campus, Div Nephrol & Hypertens, Aurora, CO USA
基金
美国国家卫生研究院;
关键词
Complement; Kidney; Glomerulonephritis; Therapeutics; HEMOLYTIC-UREMIC SYNDROME; MANNAN-BINDING LECTIN; H-RELATED PROTEINS; EXPERIMENTAL MEMBRANOUS NEPHROPATHY; DENSE DEPOSIT DISEASE; C3; GLOMERULOPATHY; ALTERNATIVE PATHWAY; IGA NEPHROPATHY; MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS; POSTINFECTIOUS GLOMERULONEPHRITIS;
D O I
10.1016/j.molimm.2020.10.015
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
It has long been known that the complement cascade is activated in various forms of glomerulonephritis. In many of these diseases, immune-complexes deposit in the glomeruli and activate the classical pathway. Researchers have also identified additional mechanisms by which complement is activated in the kidney, including diseases in which the alternative and lectin pathways are activated. The kidney appears to be particularly susceptible to activation of the alternative pathway, and this pathway has been implicated as a primary driver of atypical hemolytic uremic syndrome, C3 glomerulopathy, anti-neutrophil cytoplasmic antibody-associated vasculitis, as well as some forms of immune-complex glomerulonephritis. In this paper we review the shared and distinct mechanisms by which complement is activated in these different diseases. We also review the opportunities for using therapeutic complement inhibitors to treat kidney diseases.
引用
收藏
页码:175 / 187
页数:13
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