Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • News & Views
  • Published:

Basic research

Salt wasting in distal renal tubular acidosis—new look, old problem

Acidosis affects sodium and potassium excretion, likely via the pH sensitivity of ion transporters. A recent paper shows that β-intercalated cells with deleted H+-ATPase release ATP into urine, which induces the production of prostaglandin E2 (PGE2). PGE2 then reduces sodium absorption in the principal cells of the cortical collecting tubule and increases potassium secretion.

This is a preview of subscription content, access via your institution

Access options

Buy this article

Prices may be subject to local taxes which are calculated during checkout

References

  1. Sartorius, O. W., Roemmelt, J. C. & Pitts, R. F. The renal regulation of acid-base balance in man; the nature of the renal compensations in ammonium chloride acidosis. J. Clin. Invest. 28, 423–439 (1949).

    Article  CAS  Google Scholar 

  2. Sebastian, A., McSherry, E. & Morris, R. C. Jr. Renal potassium wasting in renal tubular acidosis (RTA): its occurrence in types 1 and 2 RTA despite sustained correction of systemic acidosis. J. Clin. Invest. 50, 667–678 (1971).

    Article  CAS  Google Scholar 

  3. Gueutin, V. et al. Renal β-intercalated cells maintain body fluid and electrolyte balance. J. Clin. Invest. 123, 4219–4231 (2013).

    Article  CAS  Google Scholar 

  4. Leviel, F. et al. The Na+-dependent chloride-bicarbonate exchanger SLC4A8 mediates an electroneutral Na+ reabsorption process in the renal cortical collecting ducts of mice. J. Clin. Invest. 120, 1627–1635 (2010).

    Article  CAS  Google Scholar 

  5. Ismail-Beigi, F. & Edelman, I. S. The mechanism of the calorigenic action of thyroid hormone. Stimulation of Na+ + K+-activated adenosinetriphosphatase activity. J. Gen. Physiol. 57, 710–722 (1971).

    Article  CAS  Google Scholar 

  6. Beauwens, R. & Al-Awqati, Q. Active H+ transport in the turtle urinary bladder. Coupling of transport to glucose oxidation. J. Gen. Physiol. 68, 421–439 (1976).

    Article  CAS  Google Scholar 

  7. Chambrey, R. et al. Renal intercalated cells are rather energized by a proton than a sodium pump. Proc. Natl Acad. Sci. USA 110, 7928–7933 (2013).

    Article  CAS  Google Scholar 

  8. Leaf, A. On the mechanism of fluid exchange of tissues in vitro. Biochem. J. 62, 241–248 (1956).

    Article  CAS  Google Scholar 

  9. Hoffmann, E. K., Lambert, I. H. & Pedersen, S. F. Physiology of cell volume regulation in vertebrates. Physiol. Rev. 89, 193–277 (2009).

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Ethics declarations

Competing interests

The author declares no competing financial interests.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Al-Awqati, Q. Salt wasting in distal renal tubular acidosis—new look, old problem. Nat Rev Nephrol 9, 712–713 (2013). https://doi.org/10.1038/nrneph.2013.235

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/nrneph.2013.235

This article is cited by

Search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing