Renal Function as a Factor in the Urinary Excretion of Ascorbic Acid.

The demonstration by Harris, Ray, and Ward (1) of a correlation between the urinary excretion of ascorbic acid and the dietary intake has led to many investigations of ascorbic acid metabolism based on the technique suggested by these authors. Sendroy and Schultz (2) have given especial attention to some of the possible factors affecting tests based on urinary excretion values. A urinary excretion test might also be affected by another factor, namely, that of kidney function. The difference between the ascorbic acid in the test dose and the amount in the urinary output has been ascribed either to a deficiency, leading to storage, or to an increased destruction of the material in the body. Nevertheless, it might be increased, especially in disease, by a lowered excretion rate. In the great majority of nutrition studies, there has probably been little error involved in the neglect of this factor, or in the tacit assumption that renal function was unvarying or normal in the cases observed. However, since such tests may and, indeed, have been applied under conditions where kidney function was undoubtedly abnormal, it seemed desirable to investigate the effect of this factor and to learn something of the mode of renal excretion of ascorbic acid. Drigalski (3), who studied a variety of pathological conditions, among which were Addison's disease, acute nephritis, and nephrosis (but one case in each condition), concluded that the excretion of ascorbic acid in the urine was independent of changes in kidney function with respect to glomerular or tubular damage. Siwe (4) studied one case of Addison's disease and found a decreased excretion of ingested ascorbic acid. Shortly thereafter, Wilkinson, Manch, and Ashford (5), studied the ascorbic acid urine excretion of three women with Addison's disease, and observed a poor response to test doses.