UniC ACID IXFAh'CTS r,4i 



these depositions, except such as can be attril)iiled to their iiieolianicul effect/' 

 but they may serve as the starting jwint of calcuU. The rejison for tlie formation 

 of these infarcts is not at all understood. Sjjienelljerg" found it iMjssible to cause 

 them experimentally in young dogs, in which they do not occur naturally, by injec- 

 tion of 0.25 gram ol uric acid per kilo. He was unable to explain why thi.s deposi- 

 tion 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 fjower of 

 infants' urine was found equal to or greater than that of adults. Other authors 

 however, have found a lower oxidative power in young aninuds, and Mendel and 

 Mitchell" have found that in the embryo pig uricolytic enzyme.^, do not appear un- 

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

 I)ower to oxidize uric acid, however, these animal experiments cannot be applied to 

 the \iric 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, 

 or from a destruction of leucocytes which is said to take place at the time of birth! 

 Flensberg believes that a hyaline substance is secreted in the urine of 'new-born 

 infants which acts as a matrix for urate deposition. McCruddcn 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.*^" Schittenhelm" found the same deposits in the 

 kidneys of rabbits fed adenine, but not when they were fed guanine. According to 

 Nicolaier," the crystals thus deposited are not uric acid or urates, but 6-amino-2-8- 

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

 oxidation. He could not find this substance in either human urine or in a uric- 

 acid calculus. Eckert''^ obtained urate deposits by intravenous injection into 

 rabbits of at least 0.08 gm. per kilo, but subcutaneous injections were ineffective; 

 injury to the renal epithelium by whatever cause interferes with this deposition of 

 urates. These experimental irifarctions are undoubtedly related to the human 

 form, and indicate that the latter depend upon the presence of an excessive amount 

 of uric acid in the infants' urine, in which a ratio of uric acid to urea of 7.9 to 74.9, 

 as against the adult ratio of about 2 to 85, was found by Sjoquist. According to 

 Niemann,^' in the first few days of life the infant excretes from 80 to 100 mg. of 

 uric acid daily, while after the fifth day the amount falls to 30 to 40 mg. daily. 

 Similar figures were obtained by Schloss and Crawford,^" who also found a corre- 

 sponding increase in the phosphoric acid, showing that the uric acid must originate 

 from nucleoproteins. The blood of fetus and mother have the same uric acid 

 content,^" but after birth the infant's blood has more during the first three or four 

 days, paralleling the high excretion." 



Adult kidneys may also show uric acid deposits in the tubules of the papilla*, 

 independent of gout. They occur as a result of cell decomposition, according to 

 M. B. Schmidt,^^ who found them especially in pneumonia, leukemia and sarcoma, 

 but not in carcinoma. 



^^ I have observed a case of fatal hematuria neonatorum, associated with most 

 extensive hemorrhagic infarction of both kidneys. In the bloody urine B. coli 

 was found in l^rge numbers. From the anatomical findings and history it seemed 

 quite possible that the injury of the kidneys by uric-acid infarcts might have 

 determined the localization of the bacteria in these organs, with resulting hemor- 

 rhages. (Trans. Chicago Path. Soc, 1909 (7), 242.) 



«2 Arch. exp. Path. u. Pharm., 1898 (41), 428. 



" Amer. Jour. Physiol, 1907 (20), 97. 



"Arch. exp. Path. u. Pharm., 1898 (41), 375. 



"" Abderhalden and Kankeleit (Zeit. exp. Med., 1916 (5), 172), have produced 

 renal deposits by feeding large amounts of tyrosine, glycine and leucineimid to 

 rabbits. These deposits consisted of the amino acid as fed, and caused suppres- 

 sion of urine by blocking up the tubules. They also caused necrosis and inflamma- 

 tory reactions. 



« Ibid., 1902 (47), 432. 



«« Zeit. klin. Med., 1902 (45), 359. 



«' Arch. exp. Path., u. Pharm., 1913 (74), 244. 



" Jahrb. f. Kinderheilk., 1910 (71), 286. 



"Amer. Jour. Dis. Children, 1911 (1), 203. 



'» Slemons and Bogert, Jour. Biol. Chem., 1917 (82), 63. 



""■ Kingsbury and Sedgwick, ibid., 1917 (31), 261. 



"2 Verb. deut. Path. Ges., 1913 (16). 329. 



