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Prof. Dr. Visith Sitprija, Department of Medicine, Chulalongkorn University Hospital, Bangkok 10500 (Thailand) Dear Sir, Failure to acidify urine in the presence of acidosis is the hallmark in the pathophysiology of distal renal tubular acidosis. Whether or not there is a defect of hydrogen ion secretion in the other systems of the body has not been explored. The interrelationship between hydrogen ion transport in the collecting tubules and gastric parietal cells thus deserves investigation. In this report we assorted to study the gastric acidity in 7 patients with primary distal renal tubular acidosis of secretory type. The patients were all female and their ages ranged from 10 to 49 years. They presented with proximal muscular weakness. The laboratory data on admission revealed serum bicarbonate ranging from 6 to 20 mmol/l, blood pH from 7.1 to 7.38, serum potassium from 1.4 to 2.6 mmol/l, serum creatinine from 44.2 to 97.3 μmol/l, and urine pH from 6.0 to 7.0. Phosphate infusion (1 mmol/l total body water) elicited the difference between urine and blood pC02 below 25 mm Hg being consistent with hydrogen ion secretion deficit [1]. Gastric analysis was performed by a standard method [2] a few weeks following alkaline treatment when hypo-kalemia and acidosis had been corrected with clinical recovery. Alkaline treatment was discontinued for 24 h before the test. A baseline gastric acidity was obtained by gastric fluid collection during 4 periods of 15 min each. This was followed by intramuscular injection of penta-gastrin (6 μg/kg) with continued gastric fluid collection for 1 h at the same interval. The maximal and peak acid secretions were calculated. The results showed low basal acid secretion when compared with the control group of 13 normal subjects. However, the difference was not statistically significant. The maximal and peak acid se-