Clinico-pathological and angio-pathological studies have been performed in 53 autopsy cases of the renal cortical necrosis, fresh renal infarcts and renal glomerular thrombosis. A detailed investigation has been carried out on the causative factors of necrotic lesions and thrombotic lesions which are resulted from circulatory derangement, and the following results are obtained.
1) Renal cortical necrosis in 12 cases out of 53 cases are encountered and among them two cases are classified in supra-super acute variety. Extensive and bilateral occurrence of the lesions are of note-worthy. The entity is frequently observed in aged group and underlying. diseases, such as malignant neoplasms, leukemia and infectious infections are also noted.
2) Fresh renal infarcts are observed in 18 cases out of 53 cases. The entity is also frequ-ently seen in aged group, suffering from heart, brain and aortic diseases from cornary, cerebral and aortic arteriosclerosis. The lesions are also tend to be multi-focal and bilateral.
3) The renal gromerular thrombosis is seen in 23 cases out of 53 cases and appear to be increasing in frequency recently. The entity is frequently observed in cases of malignant neoplasms, and septicemia. It is of interesting to note that the occurrence of the thrombosis is frequently seen in mucin-producing adenocarcinoma in malignant epithelial tumors. The abnormality of the coagulation-fibrinolysis system is justified as most important contributory factor in causation of the fibrin thrombosis. In far extensive cases of thrombosis, the secondary ischemic changes are frequently observed in renal glomeruli, however, the author justifies that the latter change is not closely related with the causation of the renal infarction.
4) The clinical investigation reveals the correlative findings of azotemia, or positive urynalysis with the degree and extent of the necrotic or thrombotic lesions. Severe anemia or visceral hemorrhage which is commonly seen in the terminal stage and eventual lowering of blood pressure may be justified as main causative factor of these disease conditions.
5) The interrelationship between the therapeutic efforts and occurrence of the renal infarctions and glomerular thrombosis should awaits further clarification in future, however, complicated and intense modes of treatment may be closely related with the increasing incidences of these conditions.
6) No essential difference of the renal cortical necrosis and renal infarctions is observed from histo-pathological point of view. The difference exists only in the extent and degree of the morbid changes in both conditions.
7) Revalent to the arterial trees in the renal infarctions, the most striking thrombo-necrotic change is discernible in the vas afferens adjacent to the glomeruli. The attention should be paid on a fact that the arterial branches of the designated lesions are involved in acute and remarkable circulatory disturbance, representing the pretlirombotic lesions. Moreover, rectus arteries, capillary vessels distributing the interstitium of the urinary tubules and veins of rather larger sizes are involved in circulatory disturbance associated with thrombus formation. The above-mentioned observation may support a view that the circulatory derangement involving the venous system is also act as important contributory fact for causation of the conditions.
8) Based on the observation, it is appropriate to justify that the theoretical basis of the functional derangement of the designated distributing arteries which is clearly defined as the "Renal ischemia with failed reflow" by Sheehan and Davis will be applied for clarifying the pathogenesis of the renal cortical necrosis and infarction. Thus it is concluded that the conditions should be explained on this theoretical basis as applied to the similar lesions in brain and heart as described by other authors in our laboratories.
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