METABOLISM IN NEPHRITIS 405 



any changes from normal in the blood pressure. Schlayer(a), after testing 

 artery strips with the blood sera of normal and hypertensive patients, 

 came to the conclusion that by this method there was no proof that there 

 is an increased suprarenal secretion that can be considered as a cause of 

 hypertension. In the discussion on carbohydrate metabolism in nephritis 

 it has already been mentioned that Neubauer suggested that epinephrin 

 in excess of normal might be responsible for the hyperglycemia character- 

 istic of some cases of Bright's disease. 



There are many further citations that could be alluded to in regard 

 to the problem of adrenal activity in relation to Bright's disease especially 

 concerning the question of hypertension. It is very tempting to believe 

 that this theory represents the actual state of affairs, as the whole matter 

 would thus be explained in a most satisfactory manner. However, until 

 definite proof of the actual occurrence of adrenalinemia is furnished by 

 the development of suitable methods, the matter must remain a theory, 

 and not an accomplished fact. It is extremely interesting to note that from 

 an experimental point of view the hypothesis of hyperadrenalinemia as 

 a cause for increased blood pressure may be entertained. Kretschmer 

 showed how small constant doses of epinephrin maintained a hypertensive 

 state in rabbits. 



Internal Secretions Derived from the Kidney. Many attempts have 

 been made to associate various manifestations of nephritis with the ab- 

 sorption of material derived from the kidney itself. Brilliant as this pos- 

 sibility is on first thought it has thus far proved itself to be more fanciful 

 than real. Great care must be exercised by those interested in this par- 

 ticular problem that a fertile imagination does not wander further from 

 the path of rational thought than the facts in the situation warrant. 



"Renin" was the term applied by Tigerstedt and Bergman (1898) to 

 a substance obtained from the rabbit's kidney which when injected into 

 animals produced a rise of blood pressure. Bingel and Strauss confirmed 

 this and Shaw enthusiastically endorsed the idea of the origin of some 

 pressor substance from the kidney itself. Bingel and Glaus, on the other 

 hand, did not find any greater amount of this product in diseased than in 

 normal kidneys and furthermore the later researches of Pearce and J. L. 

 and E. M. Miller show that the kidney does not contain a pressor substance 

 and that the internal secretion of the kidney does not furnish such a 

 material. 



From the clinical point of view it has been urged that degenerative 

 and inflammatory products resulting from corresponding processes within 

 the kidney may be responsible for hypertension. This does not agree with 

 the facts as they are known to-day for the most marked and constant ex- 

 amples of increased arterial pressure are those that are found at first as 

 hypertension without any renal involvement and in their later stages as 

 complicated by arteriosclerotic kidneys. Those forms of Bright's disease 



