1912'] A Study of the Action of Diuretics 3 



The earlier degenerations consisted in cloudy swelling and 

 vacuolation, while the later changes were principally an epithe- 

 lial desquamation, usually preceded by necrosis. 



In these late nephritides the swelling of the epithelium was 

 frequently decidedly noticeable and was sufficient either greatly 

 to encroach upon or completely occlude the lumen of the tubules. 



The present physiological study of the nephritic kidney has 

 been undertaken to determine, if possible, the part played by the 

 vascular and by the epithelial pathology of the kidney in influ- 

 encing the output of urine, and to determine whether or not the 

 vascular mechanism of the kidney is physiologically responsive 

 in a nephritis in which there is evidence of epithelial involve- 

 ment and but little histological evidence of vascular injury. 



REVIEW OF literature 



The two most important recent contributions to the study of 

 acute experimental nephritis are those by Schlayer (2) and 

 Hedinger and by Pearce (3), Hill and Eisenbrey. 



These investigations were conducted with the same general 

 object in view and are principally concerned with the physio- 

 logical response of the nephritic kidney. 



Schlayer and Hedinger studied the vascular reaction of the 

 kidney in both the glomerular and the tubular types of nephritis. 

 For their studies in the vascular type of nephritis they em- 

 ployed as kidney poisons, cantharidin, arsenic and diphtheria 

 toxin, and for the tubular type potassium chromate and corro- 

 sive sublimate. 



The investigation by Pearce, Hill and Eisenbrey was also 

 principally concerned with the vascular reaction in acute 

 nephritis. The authors were able to distinguish types of 

 nephritis in which either the tubular or the vascular changes 

 predominated. They were not able to conclude, however, that 

 a given poison produced an exclusively tubular or vascular 

 injury. Potassium chromate, corrosive sublimate and uranium 

 nitrate, caused extensive tubular injury and in the early stages 

 of the nephritis showed no evidence of vascular injury except 

 physiologically. When physiological methods were employed 

 they were able to demonstrate in the early stages of the nephritis 



