552 WASTE-PRODUCTS 



period of four additional days on a purine-free diet. The following 

 were the results obtained: 



1st period, 4th period, 



purine-free diet. 2d period. 3d period. purine-free diet. 



Total urinary N . . . 8.9 8.7 9.1 8.80 



UreaN + NH 3 . . . 7.3 7.1 7.1 7.05 



CreatinineN . . . 0.58 0.55 0.56 0.47 



Purine N (total) . . 0.11 0.17 0.26 0.10 



Uric acid 0.09 0.14 0.24 0.07 



Undetermined N . . 0.91 0.88 1.18 1.18 



The intake of purine nitrogen in the second period was 0.17 and 

 in the third 0.34 grams per day, so that the increased output only 

 accounted for one-half of the intake. The purine was not simply 

 stored, to be excreted later, for as soon as the purine-rich diet ceased 

 the excretion fell to the figure previously obtained on a purine-free diet. 

 The only alternatives that remain are either that part of the purine 

 was never absorbed from the intestine or else that the tissues of the 

 subject destroyed the purines in some manner which did not result in 

 the formation of uric acid or allantoin. We may recall the observa- 

 tions of Ascoli and Izar, cited above, which tend also to the conclusion 

 that there are means of destroying uric acid in the tissues which do 

 not involve the production of allantoin as an intermediate stage. 



In persons afflicted with Gout deposits of uric acid form in various 

 tissues and particularly in the joints. The origin of these deposits has 

 been the subject of much investigation. There is a definite increase in 

 the uric-acid content of the blood in such persons, although the uric- 

 acid output in the urine is not above the normal. Evidently, there- 

 fore, the kidneys are functioning abnormally and in such a way as to 

 constitute a barrier to the excretion of uric acid. The limiting con- 

 centration in the blood at which transmittal through the renal epi- 

 thelium begins is raised, and hence the uric acid, dammed back in the 

 blood, accumulates therein. This alone, however, is not a sufficient 

 cause of gout, for uricemia occurs also in nephritis, and in lead poison- 

 ing, without the production of gouty deposits. It has been suggested 

 that the solubility of uric acid in the blood is diminished in gouty 

 persons, but no positive evidence of this has been advanced. The 

 origin of the tendency of uric-acid deposits to form in the joints when 

 they do occur at all is, however, rendered clear by the fact upon which 

 emphasis is laid by Taylor, that Cartilage, possibly owing to its high 

 content of sodium salts, diminishes the solubility of sodium urate in 

 water, so that deposits are precipitated upon it from saturated solu- 

 tions. 



The solubilities of the monourates of potassium, sodium and ammo- 

 nium at 37 C. in water have been determined by Gudzent as follows: 



Salt of uric acid. Solubility in grams per liter. 



Potassium t t 2.7002 



Sodium 1.5043 



Ammonium 0.7413 



