How does potassium wasting occur in distal renal tubular acidosis (RTA) (type 1) 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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The serum potassium level typically is low in patients with distal RTA because defects in H+ secretion or back-diffusion of H+ tend to increase urinary K+ wasting. Potassium wasting occurs from one or more of the following factors:

  • Decreased net H+ secretion results in more Na+ reabsorption in exchange for K+ secretion.

  • The drop in serum HCO3- and, therefore, filtered HCO3-, reduces the amount of Na+ reabsorbed by the Na+/H+ exchanger in the proximal tubule, leading to mild volume depletion. The associated activation of the renin-angiotensin-aldosterone system increases K+ secretion in the collecting duct.

  • A possible defect in K+/H+ –ATPase results in decreased H+ secretion and decreased K+ reabsorption.

The serum K+ level can be high if the distal RTA is secondary to decreased luminal Na+ in the distal nephron. Na+ reabsorption in the principal cells of the collecting duct serves as the driving force for K+ secretion. In this case, the patient has hyperkalemia and acidosis; the disorder is also called voltage-dependent or hyperkalemic type 1 acidosis.

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