Deoxycholic Acid and Coronary Artery Calcification in the Chronic Renal Insufficiency Cohort

Author:

Jovanovich Anna12ORCID,Cai Xuan3ORCID,Frazier Rebecca3ORCID,Bundy Josh D.4ORCID,He Jiang4ORCID,Rao Panduranga5,Lora Claudia6,Dobre Mirela7ORCID,Go Alan8ORCID,Shafi Tariq9ORCID,Feldman Harold I.10,Rhee Eugene P.11,Miyazaki Makoto2ORCID,Isakova Tamara3ORCID,Chonchol Michel2,Appel Lawrence J.,Chen Jing,Lash James P.,Nelson Robert G.,Rahman Mahboob,Rao Panduranga S,Shah Vallabh O.,Townsend Raymond R.,Unruh Mark L.

Affiliation:

1. Renal Section VA Eastern Colorado Healthcare SystemAurora CO

2. Division of Renal Diseases and Hypertension University of Colorado Anschutz Medical Campus Aurora CO

3. Division of Nephrology/Hypertension Northwestern University Chicago IL

4. Nephrology and Hypertension Tulane University New Orleans LA

5. Division of Nephrology University of Michigan Ann Arbor MI

6. Division of Nephrology University of Illinois at Chicago Chicago IL

7. Division of Nephrology Case Western Reserve University Cleveland OH

8. Division of Research Kaiser Permanente Northern California Oakland CA

9. Division of Nephrology University of Mississippi Jackson MI

10. Division of Renal Electrolyte and Hypertension University of Pennsylvania Philadelphia PA

11. Nephrology Division Massachusetts General HospitalHarvard Medical School Boston MA

Abstract

Background Deoxycholic acid (DCA) is a secondary bile acid that may promote vascular calcification in experimental settings. Higher DCA levels were associated with prevalent coronary artery calcification (CAC) in a small group of individuals with advanced chronic kidney disease. Whether DCA levels are associated with CAC prevalence, incidence, and progression in a large and diverse population of individuals with chronic kidney disease stages 2 to 4 is unknown. Methods and Results In the CRIC (Chronic Renal Insufficiency Cohort) study, we evaluated cross‐sectional (n=1057) and longitudinal (n=672) associations between fasting serum DCA levels and computed tomographic CAC using multivariable‐adjusted regression models. The mean age was 57±12 years, 47% were women, and 41% were Black. At baseline, 64% had CAC (CAC score >0 Agatston units). In cross‐sectional analyses, models adjusted for demographics and clinical factors showed no association between DCA levels and CAC >0 compared with no CAC (prevalence ratio per 1‐SD higher log DCA, 1.08 [95% CI, 0.91–1.26). DCA was not associated with incident CAC (incidence per 1‐SD greater log DCA, 1.08 [95% CI, 0.85–1.39]) or CAC progression (risk for increase in ≥100 and ≥200 Agatston units per year per 1‐SD greater log DCA, 1.05 [95% CI, 0.84–1.31] and 1.26 [95% CI, 0.77–2.06], respectively). Conclusions Among CRIC study participants, DCA was not associated with prevalent, incident, or progression of CAC.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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