Skip to main content

Overview of Acid–Base Physiology

  • Chapter
  • First Online:
Metabolic Acidosis

Abstract

Maintenance of normal acid–base homeostasis is critical to optimal cell, organ, and whole-body function. Multiple and redundant systems, importantly those in the liver, lungs, and kidneys, work to maintain this homeostasis in the face of continuous challenges from routine metabolic processes, diet, physical activity, and illness. The liver metabolizes substances, including those ingested in the diet, to yield acid, base, or neither. The lung’s major contribution to acid–base homeostasis is excretion of “volatile” acid (carbon dioxide or CO2) whose retention increases the respiratory component of the acid–base equilibrium to cause “respiratory” acidosis. The kidney’s major contribution to this process is excretion of so-called fixed acid whose retention lowers the metabolic component of the acid–base equilibrium (bicarbonate or HCO3), causing “metabolic” acidosis. Here we provide a general overview of overall acid–base homeostasis with particular emphasis on the kidney given its important role in protecting against and sometimes causing metabolic acidosis.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 39.99
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 54.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 54.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

References

  1. Kassirer JP, Bleich HL. Rapid estimation of plasma carbonate tension from pH and total carbon dioxide content. N Engl J Med. 1965;272:1067.

    Article  CAS  PubMed  Google Scholar 

  2. Kurtz I, Maher T, Hulter HN, et al. Effect of diet on plasma acid–base composition in normal humans. Kidney Int. 1983;24:670–80.

    Article  CAS  PubMed  Google Scholar 

  3. Adeva MM, Souto G. Diet-induced metabolic acidosis. Clin Nutr. 2011;30:416–21.

    Article  CAS  PubMed  Google Scholar 

  4. Frassetto LA, Todd K, Morris Jr RC, Sebastian A. Estimation of net endogenous noncarbonic acid production in humans from diet potassium and protein contents. Am J Clin Nutr. 1998;68:576–83.

    CAS  PubMed  Google Scholar 

  5. Lemann Jr J, Bushinsky DA, Hamm LL. Bone buffering of acid and base in humans. Am J Physiol. 2003;285:F811–32.

    CAS  Google Scholar 

  6. Goodman AD, Lemann C, Lennon EJ, et al. Production, excretion and net balance of fixed acids in patients with renal acidosis. J Clin Invest. 1965;44:495–506.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  7. Remer T. Influence of nutrition on acid–base balance-metabolic aspects. Eur J Nutr. 2001;40:214–20.

    Article  CAS  PubMed  Google Scholar 

  8. Wesson DE, Simoni J, Broglio K, Sheather S. Acid retention accompanies reduced GFR in humans and increases plasma levels of endothelin and aldosterone. Am J Physiol Renal Physiol. 2011;300:F830–7.

    Article  CAS  PubMed  Google Scholar 

  9. Wesson DE, Simoni J. Increased tissue acid mediates progressive GFR decline in animals with reduced nephron mass. Kidney Int. 2009;75:929–35.

    Article  CAS  PubMed  Google Scholar 

  10. Wesson DE, Simoni J. Acid retention during kidney failure induces endothelin and aldosterone production which lead to progressive GFR decline, a situation ameliorated by alkali diet. Kidney Int. 2010;78:1128–35.

    Article  CAS  PubMed  Google Scholar 

  11. Wesson DE. Dietary acid increases blood and renal cortical acid content in rats. Am J Physiol. 1998;274[Renal Physiol. 43]:F97–103.

    Google Scholar 

  12. Sun X, Yang LV, Tiegs BC, et al. Deletion of the pH sensor GPR4 decreases renal acid excretion. J Am Soc Nephrol. 2010;21:1745–55.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  13. Swan RC, Pitts RF. Neutralization of infused acid by nephrectomized dogs. J Clin Invest. 1955;34:205–12.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  14. Lemann J, Litzow JR, Lennon EJ, et al. Studies on the mechanism by which chronic metabolic acidosis augments urinary calcium excretion in man. J Clin Invest. 1967;46:1318–28.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  15. Bushinsky DA. Net calcium efflux from live bone during chronic metabolic but not respiratory acidosis. Am J Physiol. 1989;256:F836–42.

    CAS  PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Donald E. Wesson M.D., M.B.A. .

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 2016 Springer Science+Business Media New York

About this chapter

Cite this chapter

Goraya, N., E. Wesson, D. (2016). Overview of Acid–Base Physiology. In: E. Wesson, D. (eds) Metabolic Acidosis. Springer, New York, NY. https://doi.org/10.1007/978-1-4939-3463-8_1

Download citation

  • DOI: https://doi.org/10.1007/978-1-4939-3463-8_1

  • Published:

  • Publisher Name: Springer, New York, NY

  • Print ISBN: 978-1-4939-3461-4

  • Online ISBN: 978-1-4939-3463-8

  • eBook Packages: MedicineMedicine (R0)

Publish with us

Policies and ethics