LA'/f ACJD JMWh'VTS 633 



URIC-ACID INFARCTS ■'■" 



Uric-aeitl ini'arL-ts, as the deposits of urates and urie acid observed 

 in the kidneys of at least half of all children dying within the first 

 two weeks of life are called, ^ive evidence of tlie slijihtiiess of the toxic 

 effects of these substances upon the tissues. Usually little or no 

 change occurs in the renal tubules as a result of these depositions, 

 except such as can be attributed to their mechanical effect,^^ but they 

 may serve as the starting point of calculi. The reason for the for- 

 mation of these infarcts is not at all understood. Spiegelberg ^- 

 found it possible to cause them experimentally in young dogs, in 

 which they do not occur naturally, by injection of 0.25 gram of uric 

 acid per kilo. He was unable to explain wh}^ this deposition should 

 occur in young animals but not in old, for he could not find evidence 

 of lessened oxidative power on the part of young animals, and the 

 solvent power of infants' urine was found equal to or greater than 

 that of adults. Other authors, however, have found a lower oxidative 

 power in young animals, and ^Mendel and Mitchell ^^ have found that 

 in the embryo pig uricolytic enzymes do not appear until just at or 

 just after the time of birth. As human tissues have no demonstrable 

 power to oxidize uric acid, however, these animal experiments cannot 

 be applied to the uric acid infarcts in human infants. Possibly the 

 uric-acid infarcts of infants are the result of the great destruction of 

 nucleoproteins that results from the change of the nucleated fetal red 

 corpuscles to the non-nucleated adult form. Flensburg believes that 

 a hyaline substance is secreted in the urine of new-born infants which 

 acts as a matrix for urate deposition. jMcCrudden considers the high 

 concentration of infants' urine an important factor. ^Minkowski ^^ 

 observed that administration of adenine to dogs led to a deposition of 

 uric acid or some similar substance in the kidneys. Schittenhelra ^^ 

 found the same deposits in the kidneys of rabbits fed adenine, but not 

 w^hen they w^re fed guanine. According to Nicolaier.^" the crystals 

 thus deposited are not uric acid or urates, but 6-amino-2-8-dioxy- 

 purine, derived from the adenine (6-amino-purine) by direct but in- 

 complete oxidation. He could not find this substance in either hu- 

 man urine or in a uric-acid calculus. Eckert ^'""■* obtained urate de- 



30 See discussion hy Wells and Corper, .Tour. Biol. Cliein., 1000 ((>). .')21. 



31 1 have obsej'ved a case of fatal hematuria veon-atonnti. associated with most 

 extensive hemorrha<iric infarction of both kidricvs. Tn tlic l)lnod\- urine B. coli 

 Avas found in lar<re nunilicrs. From the anatomical findin<rs and history it seemed 

 quite possil)lc tliat tlie injury of tlie kidneys by uric-acid infarcts mi£rht have 

 determined the localization of the bacteria in these orirans. with resulting 

 hemorrliages. (Trans. Chicago Path. Soc., 1000 (7), 242.) 



32Arch. exp. Path. u. Pharm., 1808 (41), 428. 



33Amer. Jour. Phvsiol.. 1007 (20), 07. 



3-t Arch. exp. Path." n. Pharm., 1808 (41), .375. 



35/&UZ., 1002 (47), 4.32. 



36Zeit. klin. Med., 1002 (4.5), 350. 



36a Arch. exp. Path. u. Pharm., 1913 (74), 244. 



