Histopathological studies on uremia were carried out by systematically investigating organs of dogs in which renal insufficiency was produced through bilateral nephrectomy and others. Groups 1 and 2, with severe renal insufficiency, were given salt, group 3, with the same condition as group 1, were given a fibrinolysin-inhibitor to inhibit vascular permeability, or not given salt, and group 4 had milder renal insufficieney than groups 1 and 2. Clinical signs were most prominent in groups 1 and 2, less prominent in group 3, and mild in group 4. Upward trend of blood pressure was observed in all the four groups.
Extensive lesions due to abnormal or increased vascular permeability were observed in organs of these experimental groups. The principal ones were : 1) fibrinoid degeneration of vascular wall, 2) exsudation of fibrin in loose connective tissue, 3) hemorrhage, 4) edema, and 5) degeneration, necrosis, dissociation and cytolysis of parenchymatous cells. There was no remarkable difference in edema between groups, but rather more prominent in groups 1 and 2. The fibrinoid degeneration, fibrin exudation, hemorrhage, and change in parenchymatous cells were generally severest in groups 1 and 2, and considerably milder in groups 3 and 4.
Fibrinoid substance, frequently observed in vascular walls of the gastrointestinal tract, urinary bladder, and gall bladder, is considered to be derived from fibrin, fibrinogen, blood plasma and its mucoprotein. From this lesion, remarkable hemorrhage and gastric and duodenal ulcers ensued.
A series of changes frequently seen in the gastrointestinal tract, urinary bladder and gall bladder, such as edema, fibrin exudation and fibrinoid degeneration are considered as the “Albuminurie ins Gewebe” developing in the process of compensatory excretion. The edema can be explained as interstitial serous inflammation, fibrin exudation as interstitial fibrinous inflammation, and fibrinoid degeneration as interstitial fibrinous inflammation as modified by the structure of vascular wall.
As the causes of the abnormal or increased vascular permeability are considered : 1) waste products in the blood as well as the metabolic disturbance of water and electrolytes in the uremic condition, 2) hypertension, and 3) activity of plasma fibrinolysin.
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