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February 4, 1961


JAMA. 1961;175(5):398. doi:10.1001/jama.1961.03040050054018

Bank and Schwartz1 call attention to the fact that intense acidification of the urine can be achieved without the induction of acidosis. Normal subjects stimulated to retain sodium showed a rapid fall in urine pH to 5.0 or below when infused with sodium sulfate. It appeared that increased reabsorption of sodium in the presence of a poorly reabsorbable anion was responsible for this phenomenon. These workers have demonstrated in experiments that during the infusion of sodium phosphate into dogs whose sodium and chloride excretion has been reduced by dietary salt restriction, excretion of titratable acid rises to near theoretical values in the presence of normal plasma bicarbonate concentrations. They suggest that a disproportion between the reabsorption of sodium and anion was the factor in regulating the acidity of the urine and the rate of excretion of titratable acid. This hypothesis was supported by the demonstration that administration of relatively

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