NITROGENOUS WASTE-PRODUCTS 553 



The solubility of sodium urate in blood is, however, no less than three 

 times its solubility in water (Taylor). This is not due to the formation 

 of diurates, since at the reaction of the blood diurates cannot exist. 

 The nature of the factor which so greatly increases the solubility of 

 uric acid is unknown. 



It was formerly considered possible to remove uric acid from the 

 body by administering Alkalies, the assumption being that the greater 

 alkalinity of the blood resulted in the formation of the more soluble 

 diurates. We now know that the alkalinity of the blood is only 

 increased to an almost imperceptible extent by this means and that the 

 maximum alkalinity attainable would not suffice to form diurates, or 

 indeed to influence perceptibly the solubility of uric acid. Nevertheless, 

 the administration of certain alkalies may be assumed to facilitate the 

 solution of uric acid by the formation of a certain proportion of the 

 more soluble potassium salt, or of the Lithium Urate which is the most 

 soluble salt of uric acid. 



The most remarkable effect upon the elimination of uric acid is, 

 however, that of phenylquinoline-carbonic acid or Atophan: 



CH c COOH 



\ 



CH 

 C CH 6 



v 



CH N 



The administration of this substance and of other quinoline-carbonic 

 acid derivatives has been shown by Nicolaier to increase the amount 

 of uric acid excreted by the kidneys to an extraordinary extent, even 

 to twice or three times the normal amount. No other physiological 

 effects are noted and no other constituent of the urine is altered in 

 amount. The increased elimination occurs on a purine-free diet and 

 has been shown by Folin and Lyman to be accompanied by a fall in 

 the uric acid content of the blood. In other words the hyperexcretion 

 of uric acid is due to the increased permeability of the kidneys for this 

 substance, just as the glycosuria following phloridzin administration 

 is due to increased permeability of the kidneys for glucose. The 

 hyperexcretion does not persist if the administration be continued, 

 the daily output sinking within a few days to only slightly above the 

 normal level, probably because the available supply of urates in the 

 blood and tissue-fluids has become exhausted. There is, however, a 

 continuous slight hyperexcretion throughout a prolonged period of 

 administration, and when nuclear tissues are administered in the diet 

 a greater proportion of uric acid is excreted in consequence than is 

 usually the case. The formation of uric acid from the nucleic acids is 

 thus facilitated by atophan, but this effect is probably only a secondary 



