330 HEKMAN O. MOSENTHAL 



muscle and the increased amounts of creatin in the blood, indicate a 

 liberation of creatin from the muscle which passes into the blood, in 

 other words, a disintegration of muscle tissue. Attention should again 

 be called to the probability that the complete or partial starvation char- 

 acteristic of the advanced nephritic state may be responsible for such an 

 increased protein katabolism and that nephritis in itself may not be the 

 cause of the protein disintegration. 



The Comparative Value of Uric Acid, Urea and 

 Creatinin in the Blood in Nephritis 



Myers and his associates have elaborated certain relationships of 

 these substances in the blood of nephritics that have proved to be of con- 

 siderable value in judging of the clinical progress of renal insufficiency 

 (Chace and Myers(fr), 1916). A high uric acid is often present when 

 there are no other signs of retention. Bauman, Ilausmann, Davis and 

 Stevens noticed the increase of uric acid content of the blood as one of the 

 earliest signs of renal insufficiency. Creatinin, on the other hand, rises 

 above the normal values in the blood only in the terminal stages of nephri- 

 tis. In making a comparison of these non-protein nitrogenous substances, 

 in the blood and urine, it was found that the kidney could concentrate the 

 creatinin one hundred times, the urea eighty times and the uric acid 

 only about twenty times. From these facts, it is evident that of these 

 three substances, creatinin is most readily eliminated by the kidney and 

 uric acid with the greatest difficulty. This makes it clear why uric acid 

 is first retained, then urea, and finally creatinin. While an increase in 

 uric acid indicates only a slight degree of renal insufficiency, a rise in 

 the blood creatinin is the signal of marked deficiency in kidney function. 

 Grouping cases of nephritis according to their severity a "staircase like" 

 picture is obtained of the increments of uric acid, urea and creatinin in 

 the blood. This is shown in Table 14. 



The above relationships are characteristic of the majority of cases of 

 nephritis. If uric acid only is increased in the blood, it must be borne in 

 mind that gout, leukemia, or other metabolic disturbance and not a renal 

 insufficiency, may be the cause for such a change. It is frequently taken 

 for granted that a rise of the blood uric acid indicates cither gout or 

 impairment of renal function. This is an unwarranted assumption, as 

 there are many instances of uric acidemia in which neither cause plays a 

 part. Until more is known concerning such conditions the figures for 

 blood uric acid must be interpreted conservatively. Dietary restrictions 

 may also be responsible for some current disturbances in these ratios. 

 Inasmuch as uric acid, and especially urea, are largely of exogenous origin, 

 and creatinin of endogenous, it follows that a low protein diet may re- 



