METABOLISM IN NEPHRITIS 391 



is the result of accelerated protein disintegration characteristic of the 

 terminal stages of Bright's disease, and in itself is a symptom rather than 

 a cause of any toxic state. 



Uric acid has here and there been referred to as a possible causative 

 agent for toxic symptoms in renal insufficiency. The fact that in both 

 gout and leukemia the nric acid may reach higher levels in the blood 

 than it will in nephritis, is sufficient evidence of the incorrectness of this 

 view. 



An old idea that potassium when retained because of renal insufficiency 

 may cause toxic symptoms has recently been revived by Smillie(.). Ob- 

 servations on man and animals were offered to support this contention. 

 Macallum found the potassium in the blood raised in a few cases of nephri- 

 tis. Recently Myers and Short again took up this problem and conclude 

 that: "The few observations reported on cases of nephritis with marked 

 nitrogen retention do not appear to support the suggestion that possibly 

 some of the symptoms of uremia are due to a potassium poisoning, as a 

 result of the retention of this element," Thus the recent reassertion of 

 the importance of potassium as a toxic substance in renal insufficiency has 

 met the same denial that was accorded it many years ago. 



Sodium Chlorid, curiously enough, has not been credited with pro- 

 ducing the asthenic symptoms characteristic of renal insufficiency, but 

 rather with those found in the convulsive type of poisoning accompanying 

 Bright's disease. It will be taken up in greater detail in the next section 

 on nephritic toxicosis. 



Indicanemia has been proposed as a cause of intoxication following 

 upon renal insufficiency by Obermayer and Popper. Here, as with all 

 substances that are retained because of deficient kidney action, the mere 

 occurrence of the substance in the blood does not furnish conclusive evi- 

 dence that it is the agent above all others that is responsible for "uremic" 

 manifestations. 



One of the few factors which has come to play a more or less definite 

 role in the poisoning brought on by renal insufficiency is acidosis. Sel- 

 lards(&), Straub and Schlayer, Peabody(c) (e), Palmer (a) (d), Chace and 

 Myers (c), and many others have pointed out that this phenomenon is 

 prone to exist when the retention of urinary excretory products becomes 

 acute. Peabody in 1915 came to the following conclusions in regard to 

 the acidosis accompanying nephritis : 



1. In mild cases of chronic nephritis, in which renal function ap- 

 proaches the normal, there is usually little or no acidosis. 



2. More advanced cases show an acidosis by the "alkali tolerance" 

 test (Sellards) but there may be no fall in the alveolar carbon dioxid 

 tension. 



