Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2018 Apr 20;10(4):512.
doi: 10.3390/nu10040512.

Dietary Treatment of Metabolic Acidosis in Chronic Kidney Disease

Affiliations
Review

Dietary Treatment of Metabolic Acidosis in Chronic Kidney Disease

Roswitha Siener. Nutrients. .

Abstract

Chronic kidney disease and reduced glomerular filtration rate are risk factors for the development of chronic metabolic acidosis. The prevention or correction of chronic metabolic acidosis has been found to slow progression of chronic kidney disease. Dietary composition can strongly affect acid⁻base balance. Major determinants of net endogenous acid production are the generation of large amounts of hydrogen ions, mostly by animal-derived protein, which is counterbalanced by the metabolism of base-producing foods like fruits and vegetables. Alkali therapy of chronic metabolic acidosis can be achieved by providing an alkali-rich diet or oral administration of alkali salts. The primary goal of dietary treatment should be to increase the proportion of fruits and vegetables and to reduce the daily protein intake to 0.8⁻1.0 g per kg body weight. Diet modifications should begin early, i.e., even in patients with moderate kidney impairment, because usual dietary habits of many developed societies contribute an increased proportion of acid equivalents due to the high intake of protein from animal sources.

Keywords: alkali citrate; bicarbonate; fruits; kidney disease; metabolic acidosis; protein; urinary stones; urolithiasis; vegetables.

PubMed Disclaimer

Conflict of interest statement

The author declares no conflict of interest.

Figures

Figure 1
Figure 1
Diurnal variation in urinary pH during a 24-h period in healthy individuals under controlled, standardized conditions before (control, blue line) and after receiving 1500 mg/day l-methionine (red line) (M ± SEM) (* p < 0.05) [31].
Figure 2
Figure 2
Diurnal variation in urinary pH during a 24-h period in healthy individuals under controlled, standardized conditions before (control, blue line) and after receiving bicarbonate-rich mineral water (red line) (M ± SEM) (* p < 0.05) [36].

References

    1. Dhondup T., Qian Q. Electrolyte and acid-base disorders in chronic kidney disease and end-stage kidney failure. Blood Purif. 2017;43:179–188. doi: 10.1159/000452725. - DOI - PubMed
    1. Rose B.D., Post T.W. Clinical Physiology of Acid-Base and Electrolyte Disorders. 5th ed. McGraw-Hill; New York, NY, USA: 2001. ISBN-10: 0071346821, ISBN-13: 9780071346825.
    1. Kazancioglu R. Risk factors for chronic kidney disease: An update. Kidney Int. Suppl. 2013;3:368–371. doi: 10.1038/kisup.2013.79. - DOI - PMC - PubMed
    1. Qian Q. Inflammation: A key contributor to the genesis and progression of chronic kidney disease. In: Ronco C., editor. Expanded Hemodialysis—Innovative Clinical Approach in Dialysis Contributions to Nephrology. Volume 191. Karger; Basel, Switzerland: 2017. pp. 77–83. - DOI - PubMed
    1. Gambaro G., Croppi E., Bushinsky D., Jaeger P., Cupisti A., Ticinesi A., Mazzaferro S., D’Addessi A., Ferraro P.M. The risk of chronic kidney disease associated with urolithiasis and its urological treatments: A review. J. Urol. 2017;198:268–273. doi: 10.1016/j.juro.2016.12.135. - DOI - PubMed

LinkOut - more resources