An augmented renal capacity to reabsorb bicarbonate (RHCO<sup>-</sup><sub>3</sub>) has been noted in patients with distal renal tubular acidosis (dRTA), and construed as evidence that the basic defect in dRTA is abnormal distal tubular permeability. According to this interpretation, the absence of a disequilibrium pH due to a back-leak of H<sub>2</sub>CO<sub>3</sub> permits increased distal H+ secretion and results in an increased RHCO<sup>-</sup><sub>3</sub>. To test this assumption, we have evaluated the effect of acute elimination of the disequilibrium pH by carbonic anhydrase infusion. The results establish that this maneuver does not cause a rise in RHCO<sup>-</sup><sub>3</sub>. Thus, the elevated value for RHCO<sup>-</sup><sub>3</sub> described in dRTA cannot be the consequence of increased back-diffusion of H<sub>2</sub>CO<sub>3</sub>, and is more likely due to coexisting extracellular volume depletion and/or potassium deficiency.