Sacks S H, Zhou W, Sheerin N S
Department of Nephrology and Transplantation, Guy's Hospital, UMDS, London, United Kingdom.
J Am Soc Nephrol. 1996 Nov;7(11):2314-9. doi: 10.1681/ASN.V7112314.
On pages 2428 to 2433 of this issue, Miyazaki et al. provide evidence that complement component C3 is synthesized within the glomeruli of patients with mesangial glomerulonephritis. Although it has been known for several years that cells isolated from the human kidney can synthesize a range of complement components, and that immune complex disease can increase the expression of these genes, it is only now that the link between intraglomerular synthesis of complement and human glomerulonephritis can be made. In view of the long interest in the role of complement in the pathogenesis of glomerulonephritis, this begs the question to what extent local complement synthesis may be involved in the generation of tissue injury. Given also the double-sided nature of complement-proinflammatory and protective-It remains to be seen if the roles of local and systemic complement differ in these respects. To weigh these questions, we examine the current evidence that connects local complement synthesis with renal injury, and ask what studies are needed to provide more definitive answers.
在本期杂志的第2428至2433页，宫崎等人提供了证据，表明系膜增生性肾小球肾炎患者的肾小球内可合成补体成分C3。虽然多年来已知从人肾分离出的细胞能够合成一系列补体成分，且免疫复合物疾病可增加这些基因的表达，但直到现在才得以建立补体的肾小球内合成与人类肾小球肾炎之间的联系。鉴于长期以来人们对补体在肾小球肾炎发病机制中的作用感兴趣，这就引出了一个问题，即局部补体合成在多大程度上可能参与组织损伤的发生。同时考虑到补体具有促炎和保护的双重性质，局部和全身补体在这些方面是否存在差异仍有待观察。为了权衡这些问题，我们审视了目前将局部补体合成与肾损伤联系起来的证据，并探讨需要哪些研究来提供更确切的答案。
