Effect of glycine loading on plasma and urinary uric acid and amino acids in normal and gouty subjects.

From the Department of Medicine, Mount Sinai School of Medicine of the City University of New York, New York 10029. These studies were supported in part by Grant-in-Aid A-162, National Institute of Arthritis and Metabolic Diseases, National Institutes of Health. Requests for reprints should be addressed to Dr. Alexander B. Gutman, Mount Sinai School of Medicine of the City University of New York, 11 East lOOth Street, New York, New York 10029. A single oral dose of glycine, 100 mg/kg body weight, a "physiologic" load, was given to ten normal men and seventeen patients with primary gout. The ensuing uricosuria, chiefly due to increased renal clearance of uric acid, was relatively greater in the gouty subjects. That the uricosuria was not due to competition between glycine and uric acid for a common reabsorptive mechanism was shown by giving probenecid, which increased renal excretion of uric acid but not of glycine or other amino acids. Pyrazinamide abolished the glycine-induced uricosuria, which is therefore assumed to be due to enhanced tubular secretion of uric acid. Glycine loading increased urinary excretion of ammonium to about the same degree in gouty and nongouty subjects; there does not seem to be any defect in utilization of glycine for renal formation of ammonia in gout. In the six normal and seven gouty subjects so examined, glycine loading evoked a similar marked increase in plasma glycine and serine, and a significant increase in urinary excretion not only of glycine and serine but also of a variety of other monoamino-monocarboxylic acids, consistent with a common tubular reabsorptive mechanism for these amino acids. The gouty subjects showed no statistically significant aberration in the response of plasma and urinary free amino acids to glycine loading.