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- Title
Complement in renal disease.
- Authors
Charlesworth, John A; Peake, Philip W; Pussell, Bruce A; Erlich, Jonathan H
- Abstract
SUMMARY: The complement system consists of a series of plasma and membrane-based proteins that participate in a wide range of biological events. These may be advantageous or damaging to the host. Most complement-mediated effects involve sequential enzymatic activity or specific receptor–ligand interactions. Many tissues synthesize complement proteins, and substantial evidence suggests that these molecules contribute to local organ function. There is a long-established link between complement and various forms of renal disease, including glomerulonephritis (GN), tubulointerstitial inflammation and transplant rejection. Among the glomerulonephritides, significant changes in plasma complement concentration are observed most commonly in acute post-streptococcal disease, mesangiocapillary GN and lupus nephritis. The pattern of abnormality may predominantly affect the classical or alternative pathway, and these changes are of diagnostic importance and, to a lesser extent, assist in monitoring disease activity. Complement deposition is demonstrable in a wide range of renal diseases, but convincing evidence of its involvement in the pathogenesis of specific diseases is quite limited. Complement reactivity also occurs during haemodialysis, and the generation of biologically active by-products has been demonstrated, to a variable extent, with different dialysis membranes. More recently, complement's involvement in the acute rejection of xenografts has been examined extensively, and attempts to modify its participation in these processes have been partially successful in experimental models. The long-term efficacy and practical value of therapeutic complement inhibition is currently under examination in a variety of human and experimental immunological disorders.
- Subjects
COMPLEMENT (Immunology); KIDNEY diseases
- Publication
Nephrology, 2001, Vol 6, Issue 4, p145
- ISSN
1320-5358
- Publication type
Article
- DOI
10.1046/j.1440-1797.2001.00057.x