Autoantibodies in human glomerulonephritis

It has often been suggested that the picture and course of human glomerulonephritis could be best explained by an antigen-antibody reaction. There are many clinical facts which support such a hy-pothesis. The interval of 10 to 20 days between the primary streptococcal infection and the first appearance of clinical signs of acute glomerulo-nephritis, the persistent absence of direct evi-dence of streptococcal invasion of the kidney itself with evidence of severe general involvement of the glomerular apparatus and the often irrevers-ible progress of the disease seem strongly to sug-gest such a possibility. In our studies on the nephrotic syndrome (1) during the last few years using the fluorescein and other methods for de-termining capillary permeability, we had the im-pression that during this stage of chronic glo-merulonephritis we are dealing with a diffuse dam-age of the entire capillary network throughout the body, possibly produced by an "allergic " reaction. Good evidence has been presented that by an an-tigen-antibody reaction a picture very similar to human glomerulonephritis and its different stages can be produced in experimental animals. Masugi (2) has shown that a chronic glomerulonephritis can be produced by the injection of a heterologous immune antikidney serum. Sarre and Wirtz (3) were able to demonstrate that such antibodies are rapidly and selectively adsorbed by the kidney and thus disappear out of the circulation, giving rise to specific changes in the kidney. They were also able to show that other organs bind these specific antibodies to a much lesser extent. Swift and Smadel (4) demonstrated the specificity of such antikidney serum by the fact that an injection of kidney extract immediately preceding the injec-tion of the antikidney serum prevented kidney damage. Injection of liver extract did not afford this protection. Burky (5) in turn showed tha