Role of Complement in Nephrotoxic Nephritis

Abstract

AN immunological mechanism has been postulated to explain some features of human glomerulonephritis¹. In acute glomerulonephritis in man and in the acute stage of experimental nephrotoxic (Masugi) nephritis the level of serum complement (C′) drops^2,3 and C′ has been demonstrated in the kidney lesions by immuno-fluorescent techniques^4,5. Since C′ is a lytic agent for some bacteria and for isolated mammalian cells ‘sensitized’ by specific antibodies, the question arises whether C′ plays an active or an incidental part in these kidney lesions. The evidence in favour of an active role is, as yet, only circumstantial, since C′ is bound in serological reactions not only when it is necessary for them, as in immune lysis, but also when it is not, as in agglutination or precipitation. More pertinent is the observation that avian antisera, reportedly poor complement fixers, usually cause nephrotoxic nephritis only after a latent period of several days, while rabbit antisera can cause it immediately⁶. The delayed nephritis has been ascribed to the rat's own antibodies against the heterologous anti-kidney anti-bodies, localized in kidneys. However, this comparison between avian and rabbit antisora is of dubious validity because of our ignorance of the serological specificity of those antisera (which may or may not be identical) as well as of their antibody content (which is usually compared only on the basis of their nephrotoxic effect—the very variable under investigation).