608 - Metabolic Acidosis Associates With Inflammation: Results From NHANES.

Publication Number: 608.5889

Denver D. Brown, Children's National Hospital, Washington, DC, United States; Douglas Lambert, Northwell Healh, Great Neck, NY, United States; James E. Bost, Children's National Hospital, Silver Spring, MD, United States; Kaye E. Brathwaite, Washington University in St. Louis School of Medicine, St. Louis, MO, United States; Rayvaughn Brown, Cornell University, New Rochelle, NY, United States; Rebecca Levy, University of Rochester School of Medicine and Dentistry, Rochester, NY, United States; Matthew Abramowitz, Albert Einstein College of Medicine, Bronx, NY, United States; Michal Melamed, New York University Grossman School of Medicine, New York, NY, United States

Background: Metabolic acidosis, a common sequelae of chronic kidney disease (CKD), has been postulated to contribute to the inflammation observed in CKD. However, the mechanisms underlying this association have yet to be fully elucidated.

Objective: This study examined the association between markers of metabolic acidosis and inflammation using cross-sectional data from the National Health and Nutrition Examination Survey (NHANES).

Design/Methods: The study population included children and adults who participated in NHANES between 1999 - 2018. The primary exposure was metabolic acidosis. This included quartiles of net endogenous acid production (NEAP), a measure of dietary acid load. Additionally, we conducted analyses using serum bicarbonate which was used categorically with low serum bicarbonate (the surrogate for metabolic acidosis) defined as < 22 mEq/L and normal serum bicarbonate defined as ≥22 mEq/L. In all analyses, the primary outcome was C- reactive protein (CRP) which was dichotomized as < 0.5 mg/dL and ≥0.5 mg/dL. We used survey-adjusted logistic regression models to examine the association between metabolic acidosis and inflammation. All models were adjusted for pertinent covariates, including age, sex, race/ethnicity, household income, body mass index (BMI), estimated glomerular filtration rate (eGFR), albuminuria (urine albumin-to-creatinine ratio, UACr).

Results: The final study cohort included 50,423 participants. Participants with CRP ≥0.5mg/dL were more likely to be female, older, overweight or obese, have slightly lower eGFR, higher UACr, and higher NEAP. Approximately 10% of the cohort had low bicarbonate levels. In unadjusted and fully adjusted analyses, increasing NEAP was significantly associated with CRP ≥0.5mg/dL- specifically, NEAP quartile 4 (the highest NEAP values) unadjusted OR 1.328 (95% CI: 1.224-1.441), fully adjusted OR 1.315 (95% CI: 1.210-1.429). In both unadjusted and fully adjusted analyses, low serum bicarbonate was associated with CRP ≥0.5mg/dL but associations did not reach significance- unadjusted OR 1.142 (95% CI: 0.999-1.305), fully adjusted OR 1.140 (95% CI: 0.996-1.304).

Conclusion(s): Using robust, nationally representative data from children and adults, we observed an association between markers of metabolic acidosis and inflammation. Metabolic acidosis is prevalent in both children and adults with CKD. There are widely available and well-tolerated treatment agents that correct metabolic acidosis. Prospective studies should evaluate whether treating metabolic acidosis modifies inflammation.