title: Net endogenous acid production is associated with a faster decline in GFR in African Americans.
abstract: Increased acid excretion may promote renal injury. To evaluate this in African Americans with hypertensive nephrosclerosis, we studied the association between the net endogenous acid production and progression of kidney disease in 632 patients in the AASK trial. Protein and potassium intakes were estimated from 24 h urea nitrogen and potassium excretion, and used to estimate net endogenous acid production, averaged over 2 years, approximating routine intake. The link between net endogenous acid production and the I(125)iothalamate glomerular filtration rate (iGFR) and time to end-stage renal disease or doubling of serum creatinine was analyzed using mixed models and Cox proportional hazards regressions. The trend in higher net endogenous acid production was significantly associated with a faster decline in iGFR over a median of 3.2 years. After adjustment for age, body mass index, baseline iGFR, urine protein-to-creatinine ratio, and randomized treatment group, the trend in higher net endogenous acid production remained significantly associated with a faster decline in iGFR at a rate of 1.01 ml/min per 1.73 m(2) per year faster in the highest compared to the lowest quartile. However, in time-to-event analyses over a median of 7.7 years, the adjusted hazard ratio (1.10) for composite renal events per 25 mEq/day higher net endogenous acid production was not significant. Hence, our findings implicate endogenous acid production as a potential modifiable risk factor for progressive kidney disease.
authors.affiliation: Department of Medicine, University of Miami, Miami, Florida 33136, USA. jscialla@med.miami.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: D000136:Acid-Base Equilibrium; D000328:Adult; D001741:Black or African American / Q000706:statistics & numerical data*; D000368:Aged; D015415:Biomarkers / Q000097:blood; D001806:Blood Urea Nitrogen; D016009:Chi-Square Distribution; D003404:Creatinine / Q000097:blood; D004044:Dietary Proteins / Q000378:metabolism; D018450:Disease Progression; D005919:Glomerular Filtration Rate; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000208:ethnology* / Q000503:physiopathology; D007483:Iothalamic Acid; D007668:Kidney / Q000378:metabolism / Q000503:physiopathology*; D007676:Kidney Failure, Chronic / Q000208:ethnology / Q000503:physiopathology; D008875:Middle Aged; D009400:Nephrosclerosis / Q000097:blood / Q000208:ethnology* / Q000503:physiopathology; D011188:Potassium / Q000097:blood; D016016:Proportional Hazards Models; D011507:Proteinuria / Q000208:ethnology / Q000503:physiopathology; D019275:Radiopharmaceuticals; D018570:Risk Assessment; D012307:Risk Factors; D013997:Time Factors; D014481:United States / Q000453:epidemiology; D055815:Young Adult
chemical_list: D015415:Biomarkers; D004044:Dietary Proteins; D019275:Radiopharmaceuticals; D007483:Iothalamic Acid; D003404:Creatinine; D011188:Potassium