Uric Acid Infarct

URIC ACID INFARCT, formation of a yellow-red deposit in the region of the renal pyramids. The washing out of this deposit by urine gives the latter a turbid appearance and causes, upon settling, the formation of a more or less abundant sediment of uric acid salts. The uric acid infarct was described as early as the 1920s of the 19th century by French authors (Bilhard, 1828), and later (in the 1840s) by German ones (Cless, Schlossberger, Virchow). It is observed in more than 50% of newborn children, from the end of the first to the fifth day of life, rarely later than a week—the "infarct period." In children who die in the first 24 hours of life, the uric acid infarct is observed significantly less frequently, and in stillbirths—as an exception. The duration of labor does not appear to affect the frequency of infarct formation. Later, in infancy, it has been found in severe nutritional disorders, and in adults in leukemia. Among animals, the uric acid infarct occurs in newborn piglets, monkeys, and certain birds. Experimentally, it has been successfully induced in newborn puppies by injecting sodium urate into their blood. There are indications that the uric acid infarct occurs more frequently with late ligation of the umbilical cord, as well as in children with jaundice. In premature and weak infants, the infarct occurs not only more frequently, but its excretion is also usually prolonged. The main causes of the formation of the uric acid infarct should be considered, on the one hand, the high content of uric acid in the urine of newborns, and on the other hand, its insufficient dissolution, which increases only gradually with the increase in the amount of fluid administered to the child. The amount of uric acid excreted by the newborn (both absolutely and relatively) is two to three times greater than that of an infant. The origin of uric acid is endogenous; however, the reasons for its abundance in the newborn are not precisely known. It is usually believed that in the blood of the newborn, which is very rich in leukocytes, the breakdown of the latter occurs, with the release of purine bases from their nuclei and the formation of uric acid from the latter. However, the "infarct period" begins earlier than the moment of decrease in the number of leukocytes, and moreover, at the present time, hyperleukocytosis in newborns is viewed as relative, considering that subsequently the process is not one of breakdown, but merely a decrease in formed elements in the blood due to an increase in its liquid parts. - The uric acid infarct in the kidney appears on its section in the form of reddish-yellow stripes in the region of the renal pyramids, extending from the cortical substance sometimes all the way to the papillae and retaining the fan-shaped arrangement of the medullary rays. According to modern views, the formation of the uric acid infarct is as follows: the epithelium of the medullary tubules secretes a hyaline substance that fills their lumens and often takes the form of cylinders; urate salts are deposited on this basis from the concentrated urine saturated with them. With increased urine secretion, the infarct masses are washed out of the tubules into the renal pelves and bladder, resulting in the characteristic urine. Under the microscope, the infarct contains cylinders, free or encrusted with salts; an irregular hyaline basis with deposits of spheres or grains of urates; urate rods, spheres, crystals of uric acid, ammonium and sodium urate, calcium oxalate; epithelial cells and leukocytes. Organic substances constitute 96.3% of the entire sediment. - The uric acid infarct should be considered a physiological phenomenon that does not cause any clinical symptoms other than the appearance of sediment in the urine, on diapers, or around the urinary opening of the child.