Clinical evidence that treatment of metabolic acidosis slows the progression of chronic kidney disease.

PURPOSE OF REVIEW: We review the growing clinical evidence that metabolic acidosis mediates chronic kidney disease (CKD) progression and that treatment to increase the associated low serum bicarbonate (HCO₃) in CKD is disease-modifying.

RECENT FINDINGS: Seven prospective studies of patients with wide ranges of estimated glomerular filtration rates (eGFRs) and serum HCO₃ examined the effect on CKD of increasing serum HCO₃ using dietary acid reduction with either oral alkali (sodium bicarbonate or sodium citrate), a vegetarian diet very low in acid-producing protein (0.3 g/kg/day) supplemented with ketoanalogues or added base-producing fruits and vegetables. Clinical outcomes included slower kidney function decline (using eGFR measurements) and fewer patients progressing to end-stage kidney disease. Post hoc analyses demonstrated that: treatment of metabolic acidosis for 2 years decreased the number of patients with at least a 40% eGFR decline, a validated surrogate for progression to end-stage kidney disease and across four studies, treatment to increase serum HCO₃ by 4-6.8 mEq/l in acidotic patients with CKD was associated with a ∼4 ml/min/1.73 m reduction in the rate of eGFR decline over 6-24 months compared with controls.

SUMMARY: Metabolic acidosis appears to enhance CKD progression and its treatment should be studied further as a potential disease-modifying intervention.