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Principal Investigator
Douglas Chang
National Institute of Diabetes and Digestive and Kidney Diseases
Position Title
Staff Clinician
About this CDAS Project
IDATA (Learn more about this study)
Project ID
Initial CDAS Request Approval
Mar 21, 2024
Comparison of net endogenous acid production from dietary self-report instruments against recovery biomarker-derived measures
Metabolic acidosis, a consequence of accumulated acid from non-respiratory sources, is typically encountered in the clinical context of advancing chronic kidney disease. However, recent studies implicate obesity (with normal kidney function) as a risk factor for clinical markers of acid accumulation (1). Markers of acid accumulation has been associated with multiple adverse health consequences including insulin resistance, metabolic syndrome, development of kidney disease, hypertension, bone disease, loss of connective and muscle tissues, and muscle weakness (2). An important contributor to acid accumulation is from dietary sources.

Epidemiological studies of nutrition have made important contributions to understanding the relationship between dietary factors and disease. Such studies rely upon tools based on self-reported dietary intake which are subject to measurement error and require validation. Advances in understanding the link between dietary acid load and health have been hampered by the limited ability to assess dietary acid load measures such as net endogenous acid production (NEAP) in the community. NEAP derived from recovery biomarkers collected from urine excretion represent an objective measure of NEAP.

The Automated Self-Administered 24-hour Dietary Assessment Tool (ASA24) is a freely available, web-based, automatically coded, self-administered recall instrument (3). How well NEAP from ASA24 and other self-reported dietary assessment tools (e.g., Diet History Questionnaire (DHQ) II; 4-d food records) compares with NEAP derived from biomarkers is unclear (4, 5).

1. Lambert DC, Abramowitz MK. Obesity, Anion Accumulation, and Anion Gap Metabolic Acidosis: A Cohort Study. Kidney360 2021;2(11):1706-15. doi: 10.34067/KID.0003562021.
2. Wieers M, Beynon-Cobb B, Visser WJ, Attaye I. Dietary acid load in health and disease. Pflugers Arch 2024. doi: 10.1007/s00424-024-02910-7.
3. Park Y, Dodd KW, Kipnis V, Thompson FE, Potischman N, Schoeller DA, Baer DJ, Midthune D, Troiano RP, Bowles H, et al. Comparison of self-reported dietary intakes from the Automated Self-Administered 24-h recall, 4-d food records, and food-frequency questionnaires against recovery biomarkers. Am J Clin Nutr 2018;107(1):80-93. doi: 10.1093/ajcn/nqx002.
4. Frassetto LA, Todd KM, Morris RC, Jr., Sebastian A. Estimation of net endogenous noncarbonic acid production in humans from diet potassium and protein contents. Am J Clin Nutr 1998;68(3):576-83. doi: 10.1093/ajcn/68.3.576.
5. Scialla JJ, Appel LJ, Astor BC, Miller ER, 3rd, Beddhu S, Woodward M, Parekh RS, Anderson CA. Estimated net endogenous acid production and serum bicarbonate in African Americans with chronic kidney disease. Clin J Am Soc Nephrol 2011;6(7):1526-32. doi: 10.2215/CJN.00150111.

To compare NEAP from self-reported dietary assessment tools (e.g., ASA24, DHQ II, and 4-d food records) against NEAP derived from urine biomarkers (e.g., calculated from 24-h urine potassium and protein excretion).


Matthew Abramowitz, M.D., M.S. (Albert Einstein College of Medicine)
Emma Stinson, M.P.H. (National Institute of Diabetes and Digestive and Kidney Diseases)
Jonathan Krakoff, M.D. (National Institute of Diabetes and Digestive and Kidney Diseases)
Heather Bowles, Ph.D. (National Cancer Institute)
Kevin Dodd, Ph.D. (National Cancer Institute)