How does distal renal tubular acidosis (RTA) (type 1) cause non-anion gap (AG) (hyperchloremic) metabolic acidosis?

Updated: Dec 08, 2020
  • Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FASN  more...
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Distal RTA (type 1) (see the Table below)

The defect in this type of RTA is a decrease in net H+ secreted by the A-type intercalated cells of the collecting duct. As mentioned previously, H+ is secreted by the apical H+ –ATPase and, to a lesser extent, by the apical K+/H+ –ATPase. The K+/H+ –ATPase seems to be more important in K+ regulation than in H+ secretion. The secreted H+ is then excreted as free ions (reflected by urine pH value) or titrated by urinary buffers, phosphate, and NH3. A decrease in the amount of H+ secreted results in a reduction in its urinary concentration (ie, increase in urine pH) and a reduction in total H+ buffered by urinary phosphate or NH3.

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