Epidemiology Etiology and Immunology

For more than 200 years, physicians have known that swelling of the face and extremities (dropsy) occurred in some individuals 10 to 14 days after bouts of scarlet fever (scarlatina). Early physicians believed that toxins, released during the fever, caused the dropsy, and long after Bright discovered the association of post-scarlatina dropsy with changes in the kidney, the role played by scarlet fever still remained a mystery. These earlier beliefs were afforded credibility with the discovery, in the latter part of the nineteenth century, that the scarlatina rash resulted from streptococcal toxins.

It was only in the latter half of the twentieth century that F. G. Germuth (1953) and F. J. Dixon and others (1961) found that rabbits developed glomerulonephritis when given injections of a foreign protein (bovine albumin). About 2 weeks after these injections, the glomerulus sustained injury from immune complexes. An immune complex consists of an antigen (the protein), an antibody (produced by the rabbit), and a complement (humoral component). Immune complexes localize in the glomerulus and damage the basement membrane. The damaged membrane leaks protein and red blood cells into the urine; swollen cells lining the capillary block the glomerular capillaries.

In humans, events mimicking this model follow certain streptococcal infections caused by "nephrito-genic" strains. Before the advent of antibiotics, glomerulonephritis usually followed an attack of scarlet fever. Today, in the Western world it more often follows streptococcal infections of the throat and skin, since scarlet fever is quite uncommon. Some part (still not identified) of the streptococcus serves as the stimulus for antibody formation.

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