Management of the Metabolic Acidosis of Chronic Kidney Disease

Adv Chronic Kidney Dis. 2017 Sep;24(5):298-304. doi: 10.1053/j.ackd.2017.06.006.


Subjects with CKD and reduced glomerular filtration rate are at risk for chronic metabolic acidosis, and CKD is its most common cause. Untreated metabolic acidosis, even in its mildest forms, is associated with increased mortality and morbidity and should therefore be treated. If reduced glomerular filtration rate or the tubule abnormality causing chronic metabolic acidosis cannot be corrected, it is typically treated with dietary acid (H+) reduction using Na+-based alkali, usually NaHCO3. Dietary H+ reduction can also be accomplished with the addition of base-producing foods such as fruits and vegetables and limiting intake of H+-producing foods like animal-sourced protein. The optimal dose of Na+-based alkali that prevents the untoward effects of metabolic acidosis while minimizing adverse effects and the appropriate combination of this traditional therapy with dietary strategies remain to be determined by ongoing studies. Recent emerging evidence supports a phenomenon of H+ retention, which precedes the development of metabolic acidosis by plasma acid-base parameters, but further studies will be needed to determine how best to identify patients with this phenomenon and whether they too should be treated with dietary H+ reduction.

Keywords: Acid; Alkali; Bicarbonate; Chronic kidney disease; Diet.

Publication types

  • Review

MeSH terms

  • Acid-Base Equilibrium
  • Acidosis / diet therapy*
  • Acidosis / drug therapy*
  • Acidosis / etiology
  • Acidosis / metabolism
  • Acidosis, Renal Tubular / drug therapy
  • Animals
  • Bicarbonates / blood
  • Diet*
  • Dietary Proteins
  • Fruit
  • Glomerular Filtration Rate
  • Humans
  • Renal Insufficiency, Chronic / complications*
  • Renal Insufficiency, Chronic / physiopathology*
  • Sodium Bicarbonate / therapeutic use*
  • Vegetables


  • Bicarbonates
  • Dietary Proteins
  • Sodium Bicarbonate