The physiological study of experimental nephritis caused by poisons of bacterial origin demonstrates that the poisons may produce types of nephritis in which either vascular or tubular changes predominate. Diphtheria toxin produces a nephritis which in its late stage is of the vascular type, but in its early stage is distinctly tubular. Tuberculin and mallein uniformly cause lesions of the tubular type, which do not pass into the vascular type.

Nephrotoxic and hemolytic immune sera cause changes in the kidneys which by physiological methods of observation present no evidence of vascular injury, but which are anatomically characterized by exudative glomerular lesions of moderate severity. This discrepancy between the results of anatomical and physiological study indicates that a lesion of the membrane controlling the passage of fluids may occur without alteration in the power of the vessels to contract and dilate. This fact is shown clearly by the lesion caused by hemolytic immune serum, which is in sharp contrast to the lesion caused by diphtheria toxin, since the latter substance not only alters the permeability of the membranes but also influences markedly the power of the vessels to contract and dilate. It is necessary therefore if the term "vascular" is used in its broadest sense, to recognize three types of vascular nephritis: (1) one in which little or no anatomical evidence of vascular injury is found, but in which physiological methods show profound vascular changes, as in arsenical nephritis; (2) one in which anatomical evidence of vascular (exudative) injury is prominent, but in which the physiological tests are negative, as in nephritis caused by a hemolytic immune serum; and (3) one in which both anatomical and physiological changes are prominent, as in diphtheria toxin nephritis.

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