THE SUGGESTION that glomerulonephritis, as seen clinically, is a manifestation of an antigen-antibody reaction was first made by Schick1 in 1907. This concept found some acceptance, although it was based at that time mostly on circumstantial evidence. Volhard2 also emphasized and endeavored to prove this theory. Additional support was given the concept when Masugi3 succeeded in producing, experimentally, a clinical and morphologic picture identical with human glomerulonephritis by injecting heterologous nephrotoxic serum. Masugi believed that the glomerulonephritis thus produced in animals was caused directly by the union of the injected antibody with the glomerular tissue, which acted as a fixed antigen. Kay,4 however, has suggested that a more complicated system is involved in the pathogenesis of nephrotoxic nephritis, since the signs of nephritis do not appear immediately upon injection of the nephrotoxic serum but only after an interval of several days. The experiments of Masugi and
LANGE K, GRAIG F, OBERMAN J, SLOBODY L, OGUR G, LoCASTO F. CHANGES IN SERUM COMPLEMENT DURING THE COURSE AND TREATMENT OF GLOMERULONEPHRITIS. AMA Arch Intern Med. 1951;88(4):433–445. doi:10.1001/archinte.1951.03810100017002
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