338 HERMAN O. MOSENTHAL 



A disintegration of protein is at times present in diabetes mellitus (Allen 

 and Du Bois). In the infectious disease it is generally appreciated that 

 destruction of protein is the rule. Its intensity apparently depends upon 

 the particular toxic causative agent and not upon any single symptom 

 such as fever. For instance, the process is much more marked in typhoid 

 fever than it is in tuberculosis. A study which has particular application 

 to the subject in hand, is that of Matz. He studied the blood chemistry 

 of cases of bronchopneumonia during an influenza epidemic at Camp 

 Travis, Texas; apparently kidney involvement in his cases played no 

 role, and yet in some instances the urea nitrogen rose as high as 148 nag. 

 per 100 c.c. of blood, the creatinin 5 mg. and the uric acid 11.8 mg. It is 

 very important to note from Matz's observations that some patients with 

 these very high values for the non-protein nitrogenous constituents in their 

 blood recovered completely. He attributes the changes to "protein in- 

 jury, disintegration and autolysis accompanying excessive lung inflam- 

 mation." The kidney, as previously stated, played no role. Phosphorus 

 and chloroform poisoning are also accompanied by increased protein dis- 

 integration (Marshall and Rowntree). Other causes of destruction of 

 body tissue might be mentioned, but it is believed that the examples cited 

 are sufficient to show that an acceleration of the process of protein destruc- 

 tion is a common occurrence, that it usually indicates the presence of a 

 serious condition, and finally that recovery may follow, even though it be 

 present. The same conclusions are probably correct in regard to the pro- 

 tein destruction that at times is found in Bright's disease. The actual 

 number of cases of nephritis in which protein disintegration has been 

 observed are exceedingly few. It has already been mentioned that this 

 process could not be demonstrated by the calorimeter. It may be of inter- 

 est to mention the results obtained in conditions more closely related to 

 Bright's disease than those detailed previously in this paragraph. In 

 experimental uranium nephritis, an increased protein destruction is often 

 present (Austin and Eisenbrey, Mosenthal(a), 1914). These results, 

 like most of those in experimental nephritis, may be interpreted in one 

 of two ways : either the symptom in question is the result of the induced 

 nephritis, or both the nephritis and the accelerated protein catabolism are 

 brought on by the same causative agent. It is much more likely that the 

 latter supposition is the correct one. Under the circumstances, it is not 

 justifiable to accept these findings as more than remotely suggestive ; the 

 situation would have an entirely different aspect if the poison or poisons 

 responsible for the production of nephritis were known and experiments 

 could be performed with them. Becker showed that in nephrectomized 

 dogs, the heaping up of non-protein nitrogen in the blood is more rapid 

 than would be caused by retention alone; he believes that the reason for 

 this is an abnormally increased protein catabolism. If Becker's conclu- 

 sion, that marked renal insufficiency may cause a disintegration of body 



