It has been shown in this paper that structural and functional changes in acute glomerular nephritis in rabbits produced by nephrotoxins by the method of Masugi are the same as those found in human glomerular nephritis. The morbid anatomy is characterized by glomerular cell proliferation, and in some cases by deposition of fibrin and crescent formation of the glomeruli and by fatty changes of the tubules. The functional changes are: oliguria, proteinuria, hematuria, cylindruria, edema, rise in blood urea, and according to Masugi (1933, 1934) and Smadel (1936, 1937), rise in blood pressure, lipuria, and fall in urea clearance and plasma proteins. As we are unaware of any discrepancies between the experimentally induced disease and human nephritis, the conclusion follows that the two so closely resemble each other that they appear to be identical.
As to the pathogenesis, it has been shown that the disease begins with a period of latency. This is characterizied anatomically by hyperemia of the glomeruli; and functionally, in at least a number of cases, by an increased diuresis. It follows, therefore, that the theory of Volhard, according to which glomerular nephritis is caused by arteriolar spasms, can no longer be maintained. It has further been demonstrated that proliferation of glomerular cells is the typical lesion, and that deposition of fibrin and crescent formation occur only in certain cases, and in these only in a widely varying number of glomeruli. As crescents are found as early as the proliferation itself, it follows that they should not be regarded as pathognomonic of the subacute phase, but that they represent a complication which probably aggravates the disease.
As to correlation of morphological and functional changes, it has been demonstrated that oliguria, marked proteinuria and diminished excretion of cyanol appear at the time when the glomerular changes are at their peak. Evidence has been presented that the oliguria and the decrease in cyanol excretion in acute glomerular nephritis are chiefly the result of the glomerular damage. It has further been demonstrated that the excretion of azofuchsin was unchanged, except for a diminution in the rabbit which at autopsy showed a marked fatty change of the tubules. We regard these observations as evidence, that, in acute glomerular nephritis in rabbits, glomeruli and tubules may function independently of each other.