Complement in renal disease

The complement system consists of a series of plasma and membrane-based pro teins that participate in a wide range of biological events. These may be a dvantageous or damaging to the host. Most complement-mediated effects invol ve sequential enzymatic activity or specific receptor-ligand interactions. Many tissues synthesize complement proteins, and substantial evidence sugge sts that these molecules contribute to local organ function. There is a lon g-established link between complement and various forms of renal disease, i ncluding glomerulonephritis (GN), tubulointerstitial inflammation and trans plant rejection. Among the glomerulonephritides, significant changes in pla sma complement concentration are observed most commonly in acute post-strep tococcal 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, ass ist in monitoring disease activity. Complement deposition is demonstrable i n a wide range of renal diseases, but convincing evidence of its involvemen t in the pathogenesis of specific diseases is quite limited. Complement rea ctivity also occurs during haemodialysis, and the generation of biologicall y active by-products has been demonstrated, to a variable extent, with diff erent dialysis membranes. More recently, complement's involvement in the ac ute 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 thera peutic complement inhibition is currently under examination in a variety of human and experimental immunological disorders.