ers have not included the ami no-acids in their analyses. Losee and Van 

 Slyke have given the ammo-acid figures as 4.4 mg. to 7.9 mg. for 

 this disease. If this figure or a figure somewhat higher, as 10 mg., is 

 taken as a fair average it will be seen that there is a rest or undetermined 

 nitrogen in the blood which, if it is justifiable'to rule out the amino-aeids 

 on the strength of these other analyses, must be a metabolite of the form 

 of oxyproteic acid or more complex form of protein. It would seem rea- 

 sonable to suppose that in this disease with the* chief and most constant 

 pathological lesion occurring in the liver that there is a failure on the 

 part of this organ to break up these metabolites to simpler forms. The 

 withdrawal of the ammonia to neutralize these substances leads to a 

 low carbon dioxid combining power of the blood or to a condition of 

 acidosis which in many respects is quite different from the acidosis present 

 in such conditions as diabetes or starvation. 



There are three possible explanations for the rise of the urea. 



1. It represents the inability of the kidney to excrete urea even at a 

 normal rate and shows a functional disturbance of this organ. 



2. Amino-acids or other proteolytic products formerly passing 

 through the placenta for the use of the fetus are refused or cease to pass 

 through that organ and therefore remain in the maternal organism and 

 are deaminized to urea. 



3. Catabolic products from autolysis of degenerated cell areas in 

 the liver, kidneys and placenta or from syncytial cell infarcts occurring in 

 the convulsive period are converted to urea. 



Increase in the Creatinin Nitrogen in the Blood 



Creatin and creatinin metabolism are independent of the ex- 

 ogenous protein metabolism when flesh is excluded from the diet. 

 Creatin is related to the mass of muscular tissue and exists in the muscle 

 plasma. It is changed by anhydration to creatinin and this occurs either 

 in the muscle or in the liver, the latter organ being usually credited with 

 this function. Ordinary muscular work does not influence the excretion 

 of the creatinin, but excessive muscular action in inanition or rapidly 

 wasting disease increases both the creatin and creatinin output. 



Creatin appears in the urine of the latter part of pregnancy and crea- 

 tinin exists in increased amounts. The increase of the creatin was ex- 

 plained by Von Hoogenhuyze and Ten Doeschate as an evidence of 

 hepatic insufficiency, but as Murlin(6) states this would call for a decrease 

 in the creatinin excreted. As there is an intimate relationship between 

 the carbohydrate and creatin metabolism, the latter author adopts a simi- 

 lar explanation to that suggested by Mendel and Rose for the presence of 

 creatin in the urine of growing children. An actual deficiency in carbo- 



