Related Experiment Videos
Unilateral Masugi nephritis in the rat
In unilateral nephritis produced in rats by clamping one kidney, injecting heterologous Masugi antiserum prepared from homogenates of cortex, and releasing the clamp after 30 to 60 minutes, nephritis develops in the unclamped kidney. In the clamped kidney, although nephritis does not occur, the injected heterologous antibody can be demonstrated in the glomeruli with immunofluorescence techniques, and the intensity increases with time. Antirat glomerular basement membrane antisera and antirat tubular fraction 3 antisera were raised separately in rabbits. Rats with one kidney pedicle clamped were injected with antirat raised separately in rabbits. Rats with one kidney pedicle clamped were injected with antirat glomerular basement membrane antiserum alone, antirat tubular fraction 3 alone, or a mixture of both. The clamp was released after 1 hour. Frozen sections of the kidney were stained at intervals for the presence of rabbit IgG and rat IgG. When antirat glomerular basement membrane was injected alone, faint linear fluorescence was noted at 24 hours in the clamped kidney, and this did not increase over 4 weeks. Antirat tubular fraction 3 antiserum injected alone showed fine granular deposits around the capillary walls at 24 hours, and the intensity of fluorescence increased with time. When a mixture of antirat glomerular basement membrane and antirat tubular fraction 3 was injected, in the clamped kidney, there was initially faint linear fluorescence. By the 8th day, a granular pattern was noted superimposed on a linear background. By 32 days, the granular pattern was evident. The presence of subepithelial deposits was confirmed by electron microscopy. It is deduced that the slow reacting factor in Masugi antiserum prepared from homogenates of cortex is partly a "contaminating" antitubular antibody and that injections of Masugi antiserum may produce two superimposed types of immunologic glomerular lesions.
In unilateral nephritis produced in rats by clamping one kidney, injecting heterologous Masugi antiserum prepared from homogenates of cortex, and releasing the clamp after 30 to 60 minutes, nephritis develops in the unclamped kidney. In the clamped kidney, although nephritis does not occur, the injected heterologous antibody can be demonstrated in the glomeruli with immunofluorescence techniques, and the intensity increases with time. Antirat glomerular basement membrane antisera and antirat tubular fraction 3 antisera were raised separately in rabbits. Rats with one kidney pedicle clamped were injected with antirat raised separately in rabbits. Rats with one kidney pedicle clamped were injected with antirat glomerular basement membrane antiserum alone, antirat tubular fraction 3 alone, or a mixture of both. The clamp was released after 1 hour. Frozen sections of the kidney were stained at intervals for the presence of rabbit IgG and rat IgG. When antirat glomerular basement membrane was injected alone, faint linear fluorescence was noted at 24 hours in the clamped kidney, and this did not increase over 4 weeks. Antirat tubular fraction 3 antiserum injected alone showed fine granular deposits around the capillary walls at 24 hours, and the intensity of fluorescence increased with time. When a mixture of antirat glomerular basement membrane and antirat tubular fraction 3 was injected, in the clamped kidney, there was initially faint linear fluorescence. By the 8th day, a granular pattern was noted superimposed on a linear background. By 32 days, the granular pattern was evident. The presence of subepithelial deposits was confirmed by electron microscopy. It is deduced that the slow reacting factor in Masugi antiserum prepared from homogenates of cortex is partly a "contaminating" antitubular antibody and that injections of Masugi antiserum may produce two superimposed types of immunologic glomerular lesions.