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JAMA. 1969;209(2):261-262.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Experimental glomerulonephritis in animals has provided a satisfactory model for studying the morphology, pathology, and immunology of the diseased kidney. It has been proved that the mesangium and the basement membrane of the glomerulus are the most vulnerable and most often affected parts. Electron microscopic examinations have provided evidence that immunoglobulin-antibody complexes seated directly on the glomerular membrane may be the factors preventing normal function and leading to illness. On the other hand, Streptococcus has been clinically implicated as a culprit in the majority of inflammatory glomerular diseases.

Freimer¹ has shown that membranes of the Streptococcus, even of its mechanically damaged L form, have a very high degree of antigenicity. Fox² proved that the M protein by its own antigenicity contributes to an increase of the virulence of certain strains of streptococci. Bleiweiss, Karakawa, and Krause³ showed how to make a preparation of streptococcal cell walls. These . . . [Full Text PDF of this Article]

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