title: Estimated net endogenous acid production and serum bicarbonate in African Americans with chronic kidney disease.
abstract: OBJECTIVE
  Metabolic acidosis may contribute to morbidity and disease progression in patients with chronic kidney disease (CKD). The ratio of dietary protein, the major source of nonvolatile acid, to dietary potassium, which is naturally bound to alkali precursors, can be used to estimate net endogenous acid production (NEAP). We tested the association between estimated NEAP and serum bicarbonate in patients with CKD.
  
  
  METHODS
  NEAP was estimated among 462 African American adults with hypertensive CKD using published equations: NEAP (mEq/d) = -10.2 + 54.5 (protein [g/d]/potassium [mEq/d]). Dietary protein and potassium intake were estimated from 24-hour urinary excretion of urea nitrogen and potassium, respectively. All of the eligible measurements during follow-up were modeled using generalized linear regression clustered by participant and adjusted for demographics, 24-hour urinary sodium, kidney function, and selected medications.
  
  
  RESULTS
  Higher NEAP was associated with lower serum bicarbonate in a graded fashion (P trend < 0.001). Serum bicarbonate was 1.27 mEq/L lower among those in the highest compared with the lowest quartile of NEAP (P < 0.001). There was a greater difference in serum bicarbonate between the highest and lowest quartiles of NEAP among patients with stage 4/5 CKD (-2.43 mEq/L, P < 0.001) compared with those with stage 2/3 disease (-0.77 mEq/L, P = 0.01; P-interaction = 0.02).
  
  
  CONCLUSIONS
  Reducing NEAP, through reduction of dietary protein and increased intake of fruits and vegetables, may prevent metabolic acidosis in patients with CKD.
authors.affiliation: Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA. jsciall1@jhmi.edu
authors.forename: Julia J
authors.initials: JJ
authors.lastname: Scialla
authors.forename: Lawrence J
authors.initials: LJ
authors.lastname: Appel
authors.forename: Brad C
authors.initials: BC
authors.lastname: Astor
authors.forename: Edgar R
authors.initials: ER
authors.lastname: Miller
authors.forename: Srinivasan
authors.initials: S
authors.lastname: Beddhu
authors.forename: Mark
authors.initials: M
authors.lastname: Woodward
authors.forename: Rulan S
authors.initials: RS
authors.lastname: Parekh
authors.forename: Cheryl A M
authors.initials: CA
authors.lastname: Anderson
mesh_terms: D000138:Acidosis / Q000097:blood / Q000208:ethnology / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D000328:Adult; D001741:Black or African American; D000368:Aged; D001639:Bicarbonates / Q000097:blood*; D016009:Chi-Square Distribution; D002908:Chronic Disease; D003430:Cross-Sectional Studies; D004044:Dietary Proteins / Q000009:adverse effects / Q000378:metabolism; D005260:Female; D005638:Fruit; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000208:ethnology; D007668:Kidney / Q000503:physiopathology; D007674:Kidney Diseases / Q000097:blood* / Q000208:ethnology* / Q000209:etiology / Q000503:physiopathology; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D008954:Models, Biological; D017419:Potassium, Dietary / Q000378:metabolism; D012964:Sodium / Q000652:urine; D014481:United States; D014675:Vegetables
chemical_list: D001639:Bicarbonates; D004044:Dietary Proteins; D017419:Potassium, Dietary; D012964:Sodium