補体系の活性化と腎組織障害―慢性腎臓病における最近の展開―

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  • 藤田 宜是
    日本大学医学部内科学系腎臓高血圧内分泌内科学分野
  • 福家 吉伸
    日本大学医学部内科学系腎臓高血圧内分泌内科学分野
  • 松本 紘一
    日本大学医学部内科学系腎臓高血圧内分泌内科学分野

書誌事項

タイトル別名
  • Contribution of Complement Activation on Kidney Injury
  • ホタイケイ ノ カッセイカ ト ジンソシキ ショウガイ マンセイ ジンゾウビョウ ニ オケル サイキン ノ テンカイ
  • ―慢性腎臓病における最近の展開―

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抄録

The complement system acts to removal exogenous pathogens, immune complexes and apoptotic cells. However, complement activation often induces tissue injury near the removal site. Complement components and these substances circulate to the kidney, and are filtrated or trapped at the glomerulus. The complement cascade is comprised of the three following pathways: the classical pathway, which is activated by the immune complex, the alternative pathway, which is activated by the inhibition of complement regulatory proteins, and the lectin pathway, which is activated by the carbohydrate terminus of glycoproteins. C5b-9 complex and C9 polymer are formed at the target tissue via any of the three pathways. Immune complexes are formed in situ within the glomerular capillary membrane, and the classical complement pathway is activated in glomerulonephritis. Circulatory C3b reacts with C3b receptors of exogenous pathogens, and the alternative complement pathway is also activated in vivo. Mannose-binding lectin and related proteins bind to the carbohydrate terminals, and the lectin pathway is activated simultaneously. Glomerular injury occurs during complement activation. Autoantibodies and circulating immune complexes are recognized in sera from systemic lupus erythematosus. Complement components in sera are consumed by complement activation. Moreover, hereditary deficiency of complement receptor 1 and the production of autoantibody against C1q are recognized in lupus nephritis. These pathological states reduce the ability to clear the immune complex, and increase the suceptibility to glomerular injury.Complement components are mainly produced in hepatocytes. The active adipocyte also produces the early components of the alternative pathway such as C3, Factor D (Adipsin), and Factor B. Thus, hypocomplementemia is recognized in emaciation and partial lipodystrophy. While hypercomplementemia is recognized in massive obesity or type 2 diabetes mellitus, and sometimes proteinuria is also recognized in these patients. In obese or diabetic patients, postprandial chylomicron activates the alternative pathway very slowly. This delayed activation, so-called ‘C3 tick over’, produces proinflammatory cytokines and induces oxidative stress in glomeruli. Complement activation is relevant in glomerular injury, not only through formation of the membrane attack complex, but also through continueous glomerular stress.

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