396 HEKMAN O. MOSENTHAL 



trimethylamin in the amounts demonstrated in uremic blood is sufficient 

 to account for the uremic convulsions." 



Cholin and neurin, Golla believes, cannot on the present evidence, be 

 accepted as poisons responsible for the convulsive symptoms attending 

 nephritis. The possibility that neurin may be the causative agent has, 

 however, not been exhausted. 



Foster(c) (1921) isolated an unidentified organic base, which was toxic 

 for guinea pigs, from the blood of patients suffering with "epileptiform 

 uremia." This poison could not be obtained from the blood of normal per- 

 sons. Foster believes that this substance may be the cause of nephritic 

 toxicosis, though he has not yet obtained it in sufficient quantities to ana- 

 lyze it. 



Ascoli supposed that the poison responsible for nephritic toxicosis 

 was to be found in nephrolysins. Various other hypotheses concerning 

 pubstances derived from the kidney have been offered but essentially they 

 amount to a statement of the particular author's belief and have nothing 

 further to recommend them. 



Hartman has advocated urinod, a substance isolated from the urine, as 

 a possible contributing factor toward nephritic toxicosis. This is a cyclic 

 compound (C 6 H 8 O) ; its exact formula is unknown. 



Summary 



What has been ordinarily described and considered as uremia has 

 been divided into three groups. 



1. Conditions hitherto often erroneously classified as uremia, notably 

 cerebral arteriosclerosis. 



2. Poisoning due to renal insufficiency, 



3. Poisoning, accompanying Bright's disease, whose characteristic 

 symptoms appear to be the result of irritation of the central nervous sys- 

 tem, which is not necessarily accompanied by renal insufficiency or re- 

 tention of urinary excretory products, and which has been termed nephritic 

 toxicosis. 



The cause of the symptoms, erroneously classified as uremia, is fre- 

 quently cerebral hemorrhages or areas of cerebral softening and possibly 

 transient cerebral ischemia due to spasm of the corresponding arteries. 



The factor which frequently brings about a fatal termination in renal 

 insufficiency is acidosis due to the retention of the acid phosphates. 



The attempts to associate either a particular substance which the kid- 

 ney excretes in insufficient amounts or some toxic material which is the 

 product of an abnormal metabolism have all been unsuccessful, with the 

 possible exception of the acidosis just alluded to. It must be recognized 

 that toxic symptoms may be produced by the sudden and excessive admin- 



