Literature DB >> 11423749

The complement system in renal diseases.

T R Welch1.   

Abstract

The complement system has long been recognized as having a role in immune glomerular disease. This review provides an update on this association, some strategies for the clinical testing of complement in disease, and a brief commentary on current research directions. Evidence of complement activation in glomerulonephritis comes from characteristic patterns of a decrease in the serum concentrations of specific components, some of which are virtually diagnostic of certain nephritides. These patterns are often accompanied by the presence of complement components in the glomeruli and the detection of complement breakdown products in the circulation. In certain diseases, circulating complement-activating substances can be detected. Although there are over 20 complement proteins, clinical analysis is most often directed at C3 and C4, with occasional measurement of B and C5. Recently, a variety of mechanisms for complement-induced injury has been recognized. These mechanisms go far beyond simple passive lysis of erythrocytes, the earliest functional effect of complement studied. The role of such mechanisms in renal disease is just beginning to be studied. Local synthesis of complement components in the kidney may play a role both in host defense and in the promotion of interstitial inflammation and scarring. Such mechanisms will likely be defined more precisely with the availability of animals with specific complement deficiencies. Ultimately, an understanding of the role of complement in renal disease may permit specific targeted inhibition of one or more complement functions as a form of therapy. Copyright 2001 S. Karger AG, Basel

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Year:  2001        PMID: 11423749     DOI: 10.1159/000045990

Source DB:  PubMed          Journal:  Nephron        ISSN: 1660-8151            Impact factor:   2.847


  5 in total

Review 1.  Role of complement 3 in the pathogenesis of hypertension.

Authors:  Lan Chen; Noboru Fukuda; Taro Matsumoto; Masanori Abe
Journal:  Hypertens Res       Date:  2019-12-18       Impact factor: 3.872

2.  Anaphylatoxin C5a contributes to the pathogenesis of cisplatin-induced nephrotoxicity.

Authors:  Hao Pan; Zhoujun Shen; Partha Mukhopadhyay; Hua Wang; Pal Pacher; Xuebin Qin; Bin Gao
Journal:  Am J Physiol Renal Physiol       Date:  2009-01-14

3.  An approach to the child with acute glomerulonephritis.

Authors:  Thomas R Welch
Journal:  Int J Pediatr       Date:  2011-11-24

4.  Increased Complement 3 With Suppression of miR-145 Induces the Synthetic Phenotype in Vascular Smooth Muscle Cells From Spontaneously Hypertensive Rats.

Authors:  Lan Chen; Noboru Fukuda; Tomoyasu Otsuki; Sho Tanaka; Yoshihiro Nakamura; Hiroki Kobayashi; Taro Matsumoto; Masanori Abe
Journal:  J Am Heart Assoc       Date:  2019-05-21       Impact factor: 5.501

5.  Immune complex glomerulonephritis following bone marrow transplantation in C3 deficient mice.

Authors:  Thomas R Welch; Lisa W Blystone
Journal:  PLoS One       Date:  2008-10-06       Impact factor: 3.240

  5 in total

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