Abstract
The rat has been used extensively as a model for human and animal renal diseases. Three types of model systems have been especially well researched.
Autologous immune-complex (AIC) nephritis (Heymann nephritis) is induced in rats by the intraperitoneal injection of the tubular brush border antigen RTEα5 and complete Freund's adjuvant. Rats develop proteinuria and proliferation of glomerular endocapillary cells as complexes of antigen and antibody lodge in glomerular basement membrane.
Nephrotoxic serum nephritis (NTS), also called Masugi nephritis, is induced in rats by administration of antiserum to rat renal structural proteins. Binding of this antiserum to glomerular basement membranes (and other proteins) causes proteinuria. As the rat produces its own antibody to the injected “foreign” antiserum, a secondary phase of damage occurs with inflammation and cellular proliferation.
Recently, there has been extensive work on anti-basement membrane nephritis in Brown-Norway rats. These rats, when immunized against heterologous glomerular and tubular basement membranes, develop florid tubulointerstitial and glomerulonephritis, with proteinuria and azotemia.
These models may be used to research basic pathogenesis of renal disease and test treatment strategies.