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Kidney Week

Abstract: FR-PO285

Deoxycholic Acid (DCA) and Coronary Artery Calcification (CAC) in the Chronic Renal Insufficiency Cohort (CRIC)

Session Information

Category: CKD (Non-Dialysis)

  • 2101 CKD (Non-Dialysis): Epidemiology, Risk Factors, and Prevention


  • Jovanovich, Anna Jeanette, Denver VA / University of Colorado, Denver, Colorado, United States
  • Cai, Xuan, Northwestern University, Chicago, Illinois, United States
  • Frazier, Rebecca, Northwestern, Chicago, Illinois, United States
  • Bundy, Joshua David, Northwestern University Feinberg School of Medicine, Evanston, Illinois, United States
  • He, Jiang, Tulane School of Public Health and Tropical Medicine, New Orleans, Louisiana, United States
  • Rao, Panduranga S., University of Michigan Health System, Ann Arbor, Michigan, United States
  • Lora, Claudia M., University of Illinois at Chicago, Chicago, Illinois, United States
  • Dobre, Mirela A., Case Western Reserve University, Cleveland, Ohio, United States
  • Go, Alan S., Kaiser Permanente Northern California, Oakland, California, United States
  • Shafi, Tariq, University of Mississippi Medical Center, Jackson, Mississippi, United States
  • Feldman, Harold I., University of Pennsylvania, Philadelphia, Pennsylvania, United States
  • Rhee, Eugene P., Massachusetts General Hospital, Newton, Massachusetts, United States
  • Chonchol, Michel, University of Colorado, Aurora, Colorado, United States
  • Miyazaki, Makoto, University of Colorado-Denver, Aurora, Colorado, United States
  • Isakova, Tamara, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States

Circulating levels of the secondary bile acid, DCA, are elevated in chronic kidney disease (CKD). In a small cohort of individuals with CKD 3b-4, higher plasma DCA was associated with prevalent CAC. Whether circulating DCA levels are associated with CAC prevalence, incidence, and progression in a large diverse CKD population is unknown.


We cross-sectionally and longitudinally evaluated the association between fasting serum DCA levels and CAC among 1057 CRIC participants using multivariable-adjusted regression models. CAC was measured in Agatston units at baseline and follow-up.


Mean age was 57±12 years, 47% were female, and 41% were black. At baseline 676 (64%) had any CAC (CAC score >0 Agatston units), 405 (38%) had CAC >100, and 236 (22%) had CAC >400. In cross-sectional analyses, multivariable models adjusted for demographics and clinical factors including statin use showed no significant association between circulating DCA levels and CAC >0 compared to no CAC (CAC=0) (prevalence ratio per 1-SD increase in log DCA: 1.09, 95% CI 0.92-1.28). Similar results were observed when baseline CAC thresholds of >100, >200, >300, and >400 vs. no CAC (CAC=0) were used. 672 participants had follow-up CAC measurements. Over a mean follow-up of 3.2±0.6 years, of the 277 (41%) participants with no baseline CAC (CAC=0), 60 (22%) developed incident CAC (CAC >0). In the fully adjusted model, DCA was not significantly associated with incident CAC (CAC >0) (incidence ratio per 1-SD increase in log DCA: 1.06, 95% CI 0.83-1.34). Of the 395 (59%) participants with any baseline CAC (CAC >0), 20% and 7% had an increase of >100 and >200 Agatston units/year, respectively, at follow-up. In the fully adjusted model, DCA was not associated with CAC progression (risk ratio for increase in >100 and >200 Agatston units/year per 1-SD increase in log DCA: 1.08, 95% 0.87-1.34 and 1.18, 95% CI 0.77-1.82, respectively).


In CRIC participants, DCA was not associated with prevalent, incident, or progression of CAC.


  • NIDDK Support