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Acidification of the urine and urinary excretion of hydrogen was studied in ten gouty subjects (age 24–56, mean 38) with normal renal function. In three gouty patients on low purine intake, urinary pH and net acid excretion were not different from that found in normal controls. Furthermore, the response to ammonium chloride load was similar in both groups. In contrast, gouty patients on high purine intake showed permanent aciduria with lowered ammonium excretion and a diminished response to ammonium chloride load. In the four gouty subjects given ammonium chloride during high purine intake, mean urinary uric acid excretion decreased by 300 mg. day while serum urate did not change. This decrement was closely related to the progressive increase in urinary ammonium. Three gouty subjects given equivalent amount of dilute hydrochloric acid failed to show a similar response. The present study indicates that protein and purine intake may influence urinary acidification in primary gout. The data further suggest a possible relationship between ammonia and uric acid production during high purine intake and ammonium chloride load.