METABOLISM IN NEPHRITIS 395 



Sodium clilorid has at times been accorded the blame for toxic mani- 

 festations accompanying Bright's disease. The one author usually cited 

 as declaring in favor of this theory is Bohne, who came to his conclusions 

 after injecting salt into animals. Hofmann, with good reason, criticizes 

 these experiments and does not see why sodium chlorid and uremia should 

 be regarded as cause and effect. That an excess of salt in the body will 

 result in severe symptoms may be seen in the following instructive case 

 report of Campbell (quoted by Volhard). Through an error a boy of five 

 years received a rectal injection of water containing 450 gm. of salt per 

 liter; headache, thirst, vomiting and bloody stools came on rapidly ; within 

 one half hour there was unconsciousness and within 5 hours, after many 

 convulsions, the patient died. In regard to salt, as is true for many sub- 

 stances, almost any side of the uremic question may be given a semblance 

 of probability if experiments are properly devised. The researches of 

 Griinwald may be cited as demonstrating the exact opposite of what Camp- 

 bell's fatal case would indicate. Griinwald found that rabbits fed on a 

 diet very low in chlorin give up an excess of chlorids after diuretin ; such 

 a loss of salt results in convulsions and death. Widal, according to the 

 substances retained by an insufficient kidney, divided renal disturbances 

 into two classes, the chloremic and the azotemic types. The symptoms 

 characteristic of the latter brought on by an increase of urea and other pro- 

 tein derivatives are those found in the disease described in the previous 

 section under the heading of renal insufficiency. In the chloremic type, 

 symptoms characteristic of the nephritic (convulsive) toxemia may be 

 present. These are explained by assuming that the salt and water reten- 

 tion bring about edema of the lungs, gastro-intestinal tract, central nervous 

 system, etc., and thus are responsible for dyspnea, vomiting, diarrhea, 

 headache, Cheyne-Stokes' breathing, convulsive seizures, etc. That the 

 symptoms of irritation of the central nervous system are not necessarily 

 associated with cerebral edema has already been shown in the section giv- 

 ing Cohnheim's views in 1882 ; furthermore, some of the nephritic toxemias 

 exhibit their symptoms in the absence of edema. To ascribe convul- 

 sive seizures, etc., to the mechanical effect of water retention induced by 

 insufficient salt elimination does not meet the objections previously out- 

 lined, and sodium chlorid cannot be considered to be the sole cause of 

 nephritic toxemia. 



Golla, working on the theory that the convulsive and other phenomena 

 in the nephritic patient should be due to some body formed as a result 

 of abnormal metabolism, took up the problem of further investigation of 

 trimethylamin in nephritis. He demonstrated a considerable increase of 

 trimethylamin in the blood of uremics and a slight increase in the urinary 

 output. His final conclusion may be given in his own words: "It is, 

 however, hard to believe, even allowing for long continued action, that 



