[Dietary control of metabolic acidosis in chronic kidney disease]

Abstract

Metabolic acidosis is a frequent complication of chronic kidney disease. Although it is known to appear at advanced stages, many studies suggest a state of "global protonic retention" starting at early stages of the disease, responsible of tissue damage, particularly musculoskeletal, alteration of protidic metabolism and endocrine disorders, promoting malnutrition and chronic inflammation, and finally increasing mortality. The majority of international recommandations suggest of supplementation by alkali, most of the time by sodium bicarbonate, to struggle against this complication. An interesting alternative to correct acidosis would consist on the modulation of the endogenous production of acid by playing with the alimentary incomes. In fact, it has been demonstrated that some different types of food produce or consume protons during their metabolism. Low protein diet and rich fresh fruits and vegetables diet would manage to correct at least as well as the supplementation by sodium bicarbonate the metabolic acidosis, and to struggle against its complications, noteworthy by slowing the decline of glomerular filtration rate by limiting the toxic adaptative fibrotic mechanisms, demonstrated by the decrease of urinary tubulo-interstitial suffering markers. Of the condition of being well led, those diets do not seem to expose patients to an over-risk of malnutrition or hyperkaliemia. They therefore appear to be an attractive alternative, efficiency and safe, to fight against chronic kidney disease metabolic acidosis and its complications.

Keywords: Acidose métabolique; Alcalinisation; Alkalinization; Charge acide alimentaire; Charge acide rénale potentielle; Chronic kidney disease; Céto-analogue; Dietary; Dietary acid load; Diététique; Excrétion nette d’acide; Fresh fruits and vegetables; Fruits et légumes frais; Insuffisance rénale chronique; Keto-analogue; Low protein diet; Metabolic acidosis; Net acid excretion; Net endogenous acid production; Potential renal acid load; Production d’acides endogènes nette; Régime hypoprotidique.