328 HERMAN O. MOSENTHAL 



tion of creatin in the blood has no great clinical value at present, hut may 

 be of considerable importance in determining the course of protein metab- 

 olism in this disease. 



Under normal conditions (excepting in children, and at times in 

 women) there is no creatin in the urine while the creatin in the blood at- 

 tains a level of 3.5 to (5 mg. per 100 c.c. (Folin and Wu). The greater 

 portion of the blood creatin is contained in the corpuscles; only a slight 

 amount is present in the plasma (Hunter and Campbell). It is the 

 quantity of the creatin in the plasma, according to Hunter and Campbell, 

 which determines the presence or absence of creatinuria. Whenever the 

 plasma creatin (uncorrected figures) is lower than 1.4 mg. per 100 c.c., 

 the urine is creatin free ; when it is above 3.2 mg., creatinuria appears. 

 The term "uncorrected figures" applies to results obtained with Folin's 

 original method, which is not reliable for the determination of blood 

 creatin, but furnishes data which are about double the true value; how- 

 ever, until other observations are forthcoming they may be accepted as 

 having a "provisional validity." All the figures given in this section 

 were obtained by this method. 



Two deductions of considerable significance may be made from the 

 above facts. First, that the absence or presence of creatin in the urine 

 is largely a matter of the level of the kidney threshold to this substance 

 in the plasma and not, as has been frequently taken for granted, solely a 

 problem of metabolism ; second, that, inasmuch as the creatin in the blood 

 is not eliminated, the body must possess the power of destroying it. An 

 accumulation of creatin in the blood would therefore be due to a dimin- 

 ished ability of the body to change creatin chemically or to an increased 

 production of creatin. The former probably does not take place, and the 

 latter is much the more likely occurrence. An increased formation of 

 creatin is now generally acknowledged to be associated with the destruc- 

 tion of muscle protein (see section on creatin metabolism). A rise in, 

 the blood creatin in nephritis would therefore indicate an accelerated dis- 

 integration of protein, especially of muscle protein. 



The few available observations indicate that the blood creatin rises 

 when renal insufficiency exists. Myers and Fine (c)(1915) found the 

 creatin content of nephritic blood to be as high as 31.4 mg. per 100 gm. ; 

 in the author's series it reached the level of 26.9 mg. These are terminal 

 cases. Earlier in the disease, it is usual for the blood creatin to show in- 

 crements of less marked degree (see table 12). If the present theories of 

 creatin metabolism are correct, these facts indicate that a destruction of 

 protein commonly occurs in nephritis and, to a less extent, in other dis- 

 eases associated with renal insufficiency. The amount of protein catab- 

 olism above the normal is too slight to be detected by calorimetric de- 

 terminations (see section on the utilization of proteins in nephritis). It 

 does not necessarily follow that this slight increase in protein catabolism 



