Oxaluria

Oxaluria, in the literal sense, is the excretion of calcium oxalate with the urine - a phenomenon observed in the norm, but usually under O. is implied an increased excretion of calcium oxalate. Oxaluria has long been noted in diabetes mellitus, obesity, and gout. Thanks to this, oxaluria was considered a special disease and was included in the number of disorders of metabolism. Even a characteristic clinical picture for oxaluria with the presence of a number of neurasthenic symptoms was described. At present, the significance of oxaluria is limited to cases where it can be linked to the formation of urinary stones. The amount of oxalic acid excreted in the norm is equal to 15-20 mg pro die. The origin of oxaluria can depend both on the nature of food substances containing oxalic acid and on its formation inside the organism (intestine?) in the process of normal metabolism. Some nutrients are quite rich in oxalic acid content (asparagus, beans, sorrel, radish, beets, tomatoes, oranges, grapes, etc.). The endogenous part of oxalic acid represents only a small part of the oxalates excreted with the urine. The place and method of formation of oxalic acid in the organism cannot be traced with accuracy. The assumption about the origin of oxalic acid from carbohydrates is based on the fact that upon the introduction of carbohydrates, the amount of oxalates excreted increases. Fürbringer and Naunin found very sharp oxaluria in diabetes. In the case of Fürbringer, diabetes was combined with aspergillosis and gangrene of the lungs. Crystals of calcium oxalate were found in this case also in the sputum. This combination represents great interest for understanding the essence of oxaluria, if one takes into account that Aspergillus niger converts sugar into oxalic acid. Most authors, however, deny the connection of oxaluria with a disturbance of carbohydrate metabolism. Oxaluria upon feeding with carbohydrates apparently stands in connection with a change in the bacterial flora of the intestine, which takes place with carbohydrate feeding. Oxaluria is observed during processes of putrefaction in the intestine, during its catarrhal states, during diarrheas (Fürbringer). Rosenberg found a huge amount of oxalates in the urine during enteritis (up to 1246 mg on an oxalate-free diet). Increased excretion of oxalates is also observed in typhoid fever. De Sandro isolated a special bacterium from the feces which converts carbohydrates into oxalic acid (Bacterium oxalatigenum). Oxaluria is also observed in catarrhal and obstructive jaundices, and with the restoration of bile excretion into the intestine, simultaneously with the staining of the feces, the amount of oxalates in the urine decreases again. Klemperer and Tritschler introduced glycocholic acid sodium to dogs and noted an increase in the amount of oxalates in the urine. However, these experiments do not bring clarity into the mechanism of formation of oxalic acid in the organism and into the understanding of the connection of its endogenous formation with bile excretion, because oxaluria can also depend on the influence of bile on the bacteria of the intestine. Some authors consider the formation of oxalic acid from creatinine possible. Feeding with gelatin gives an increase in the amount of oxalates in the urine, which is linked to the influence of glycolic acid, the content of which in gelatin fluctuates from 16.5% to 19.25%. The connection of oxaluria with protein metabolism also cannot be considered proven. The connection of oxaluria with purine metabolism is also not proven. In acute manifestations of gout, the excretion of oxalates is often not increased; similarly, in acute oxaluria, one cannot establish a constant increase in the amount of uric acid in the urine or blood. In leukemias, as well as in pneumonia during the recovery period, during the period of increased excretion of uric acid, oxaluria is not observed. Upon the introduction of alkalis with food, the amount of oxalates in the urine falls. Upon the introduction of HCl and salicylic acid (salicylates), the excretion of oxalates increases. Of 100 mg of pure oxalic acid introduced into the organism, about 15 mg is excreted with the urine, 10 mg with the feces, and the excretion of the remaining 75 mg cannot be detected; they are destroyed in the organism, mainly in the intestine. The amount of oxalates excreted is usually judged by the amount of calcium oxalate crystals in the sediment of the urine (see Urine). They are found in the urine with an acidic, neutral, and alkaline reaction. However, this judgment is unreliable: in addition to insoluble calcium salts, other more or less soluble salts of oxalic acid are also excreted with the urine (magnesian, etc.). Umber, for example, cites a case where with 7.5 mg% of oxalic acid, not a single crystal of calcium oxalate could be found. - Thanks to its insolubility, the calcium salt can serve as material for the formation of hard and sharp stones, which easily injure the mucous membrane and often cause pain and bleeding (see Stone disease and Bladder, bladder stones). It is necessary only to note that the formation of urinary stones is connected not only with an increased excretion of salts. Salts of oxalic acid, as well as other salts (uric, phosphoric, and carbonic), are found in the urine in a concentration significantly exceeding their solubility in water. The precipitation of these salts from the solution is a secondary phenomenon, connected with a change in the reaction of the urine, its colloidal state, the ratio of Ca and Mg salts. Consequently, it is not so much the amount of oxalates introduced that plays a role, as changes in the conditions influencing their retention in the solution. For this reason, the quantitative determination of the excreted oxalic acid salt also has no practical significance.