title: Acid-base status and progression of chronic kidney disease.
abstract: OBJECTIVE
  Most patients with reduced glomerular filtration rate (GFR) have progressive GFR decline despite currently recommended kidney-protective interventions. Recent studies support that dietary acid reduction with Na(+)-based alkali or food types that yield base when metabolized provides kidney protection that is additive to currently recommended interventions. We review these recent studies in light of current kidney-protective recommendations for chronic kidney disease (CKD).
  
  
  RESULTS
  Animal models of CKD show that metabolic acidosis and/or dietary acid induce intrakidney mechanisms that cause kidney injury and mediate progressive GFR decline. Translational studies in patients show that NaHCO(3) ameliorates kidney injury in patients with CKD and reduced GFR, with and without metabolic acidosis; NaHCO(3) and base-inducing food types each ameliorate kidney injury in patients with reduced GFR without metabolic acidosis; and NaHCO(3) and Na(+) citrate each slow GFR decline in CKD patients with reduced GFR, with and without metabolic acidosis.
  
  
  CONCLUSIONS
  Recently published studies in animals and humans suggest that acid-base-related mechanisms mediate nephropathy progression. These studies support that dietary acid reduction with Na(+)-based alkali or alkali-inducing food is an effective kidney-protective adjunct to current strategies and support re-examination of current recommendations for CKD management.
authors.affiliation: Departments of Internal Medicine, Texas A&M Health Sciences Center College of Medicine, Temple, Texas, USA.
authors.forename: Nimrit
authors.initials: N
authors.lastname: Goraya
authors.forename: Donald E
authors.initials: DE
authors.lastname: Wesson
mesh_terms: D000136:Acid-Base Equilibrium / Q000502:physiology*; D000138:Acidosis / Q000378:metabolism; D000818:Animals; D004032:Diet; D018450:Disease Progression; D005919:Glomerular Filtration Rate; D006801:Humans; D051436:Renal Insufficiency, Chronic / Q000175:diagnosis / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology