METABOLISM IN NEPHRITIS 397 



istration of almost any material contained in the body. Thus a number 

 of investigators have found that injections of large amounts of urea are 

 fatal (Hammond, Grehaut and Quinquaud, Herter and Wakeman(a)) ; 

 even such symptoms as vomiting, restlessness, opisthotonic convulsions, 

 rapid respirations, coma and death were produced in such experiments 

 (Marshall and Davis). Yet, judging the effect -of urea from the clinical 

 point of view, this substance will not result in untoward symptoms. The 

 same apparent discrepancy may be noted in regard to the much quoted 

 experiments of Landois. He found that creatin, urates, etc., applied to the 

 cerebral cortex caused convulsive seizures and coma in animals. The con- 

 clusion which may be drawn from these facts is that the accumulation of 

 various crystalloids in the blood and tissues may result in disturbed osmotic 

 relations that produce the symptoms considered to be characteristic of 

 uremia. It is perfectly obvious that the rapid rise in such substances may 

 produce effects that will not be manifest if they accumulate slowly and 

 allow adjustments in the osmotic processes of the body to establish them- 

 selves. This explains the difference between injection and ingestion ex- 

 periments and the clinical phenomena accompanying renal insufficiency. 

 Such osmotic effects of heaped up crvstalloids in the body may be a con- 

 tributory factor in the poisoning characteristic of renal insufficiency. 



The cause for nephritic toxicosis evidently has not been determined or 

 even remotely approached. However, this appears to be certain, that the 

 same factor which results in the toxic (uremic) symptoms in this form of 

 poisoning is also responsible for the nephritis, and that the toxic symptoms 

 are not dependent upon the renal disease, as has been so frequently as- 

 sumed. In other words both the Bright's disease and nephritic toxicosis 

 are brought on by the same metabolic disturbance of unknown nature. 



Increased Arterial Pressure in Nephritis 



An increased blood pressure has been regarded as a characteristic sign 

 of nephritis ever since Bright (c), in 1836, noted that cardiac hypertrophy 

 and dilatation accompanied diseases of the kidney. It has been thought 

 that such a blood pressure was a phenomenon which compensated for dimin- 

 ished kidney function by forcing the renal parenchyma to greater activity. 

 This is the obvious conclusion that is necessarily come to at first glance. 

 As clinical and experimental evidence have accumulated it has become 

 evident that this interpretation is incorrect and that another solution of 

 this problem must be looked for. 



There are two considerations that make it doubtful whether a discus- 

 sion of increased arterial pressure should be taken up in an article on the 

 metabolism of nephritis. In the first place, the cause of hypertension may 

 possibly not be dependent upon a metabolic disturbance, and in the second 



