389 



and when coma has supervened may point to the true cause of the uncon- 

 sciousness making a differential diagnosis (for instance from the coma 

 accompanying cerebral hemorrhage) possible. Furthermore, it should be 

 mentioned (see section on hypertension) that in some of these cases there 

 is a slight rise in blood pressure. Janeway reported a systolic pressure 

 of 180 mm. of mercury in a man whose only kidney had been removed; 

 various observers have noted an increase in arterial pressure accompanying 

 anuria or marked oliguria from any cause whatsoever, though it is not a 

 constant symptom. In one recent case of ureteral obstruction due to car- 

 cinomatous involvement of the bladder and ureters, the systolic blood pres- 

 sure was 130 mm. of mercury. 



''With Blum we may distinguish uremia, i. e., the effects due to toxic 

 products of metabolism before their passage through the kidney, and uro- 

 toxemia, the absorption of urinary toxic bodies after their passage through 

 the kidney. Now any condition of urinary obstruction must be a com- 

 pound of these two forms of intoxication" (Golla). Much time and 

 effort has been spent in elucidating the above fascinating theory. So far no 

 proof has been brought that the toxicity of retained materials due to 

 urethral obstruction is different from that brought on by double nephrec- 

 tomy. The final demonstration of this fact was brought by the uretero- 

 venous anastomoses performed by Reid upon dogs. The writer carried 

 out double nephrectomy in other animals in the same laboratory and noted 

 that the dcgs without kidneys, and those excreting their urine into their 

 own veins, died with the same symptoms, after the same interval, and 

 gave no evidences of significant differences in their blood chemistry. It 

 may therefore be concluded that the kidney does not intensify the toxicity 

 of the waste products it excretes. Why this should ever have been sup- 

 posed to be so is another matter. 



Innumerable animal experiments in which the ureters or renal vessels 

 have been tied, the kidneys partially or completely extirpated or uretero- 

 venous anastomoses performed (Reid) have failed to produce the much de- 

 sired convulsive form of uremia. The animals have invariably become 

 drowsy, then comatose and finally died. The human symptoms and those 

 in animals have proved to be identical. These results have made it per- 

 fectly clear that anuria or markedly insufficient kidney action brings about 

 a definite clinical picture ; whether a single substance, of the many renal 

 excretory products retained, is responsible for this state, or whether all of 

 them combined bring it about, remains to be determined. It is only 

 natural that the search has been directed towards a single chemical factor 

 that may be responsible for this form of uremic coma. 



Urea has been the substance most frequently considered to be the cause 

 of uremia, ever since Babington in 1836 found this material to be in- 

 creased in the blood during renal insufficiency. Since that time Frerichs 

 advanced his brilliant but untenable theory that the toxic material was 



