Format

Send to

Choose Destination
Curr Opin Nephrol Hypertens. 2018 Mar;27(2):94-101. doi: 10.1097/MNH.0000000000000386.

Retarding progression of chronic kidney disease: use of modalities that counter acid retention.

Kraut JA1,2,3,4, Madias NE5,6.

Author information

1
Medical and Research Services, VHAGLA Healthcare System.
2
UCLA Membrane Biology Laboratory.
3
Division of Nephrology, VHAGLA Healthcare System.
4
David Geffen School of Medicine, Los Angeles, California.
5
Division of Nephrology, Department of Medicine, St. Elizabeth's Medical Center.
6
Department of Medicine, Tufts University School of Medicine, Boston, Massachusetts, USA.

Abstract

PURPOSE OF REVIEW:

Acid retention because of chronic kidney disease (CKD) increases tissue acidity and accelerates progression of CKD, whereas reduction in acid retention slows progression of CKD. Herein, we describe the mechanisms through which increased tissue acidity worsens CKD, modalities for countering acid retention and their impact on progression of CKD, and current recommendations for therapy.

RECENT FINDINGS:

Studies in animals and humans show that increased tissue acidity raises the renal levels of endothelin, angiotensin II, aldosterone, and ammoniagenesis, thereby worsening renal fibrosis and causing progression of CKD. Measures that counter acid retention, such as providing alkali or modifying the quantity or type of dietary protein, reduce the levels of endothelin, angiotensin II, aldosterone, and ammoniagenesis, slowing progression of CKD. Alkali can be provided as NaHCO3, sodium citrate, or base in fruits and vegetables. A serum [HCO3] of 24-26 mEq/l is targeted, because higher values can be associated with adverse consequences.

SUMMARY:

Insights into the mechanisms through which increased tissue acidity mediates progression of CKD and the beneficial impact of ameliorating positive acid balance underlie our recommendation for modalities that counter acid retention in CKD.

PMID:
29140821
DOI:
10.1097/MNH.0000000000000386
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wolters Kluwer
Loading ...
Support Center