Estimated net endogenous acid production and serum bicarbonate in African Americans with chronic kidney disease.

Published

Journal Article

BACKGROUND AND OBJECTIVES: 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. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: 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.

Full Text

Duke Authors

Cited Authors

  • Scialla, JJ; Appel, LJ; Astor, BC; Miller, ER; Beddhu, S; Woodward, M; Parekh, RS; Anderson, CAM

Published Date

  • July 2011

Published In

Volume / Issue

  • 6 / 7

Start / End Page

  • 1526 - 1532

PubMed ID

  • 21700817

Pubmed Central ID

  • 21700817

Electronic International Standard Serial Number (EISSN)

  • 1555-905X

Digital Object Identifier (DOI)

  • 10.2215/CJN.00150111

Language

  • eng

Conference Location

  • United States