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Abstract: TH-OR025

Serum Bicarbonate Level and Coronary Artery Calcification – A Report from the Chronic Renal Insufficiency Cohort (CRIC) Study

Session Information

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical


  • Dobre, Mirela A., Case Western Reserve University, Cleveland, Ohio, United States
  • Patel, Neil H., Case Western Reserve University, Cleveland, Ohio, United States
  • Yang, Wei, University of Pennsylvania, Philadelphia, Pennsylvania, United States
  • Chen, Jing, Tulane School of Medicine, New Orleans, Louisiana, United States
  • Hamm, L. Lee, Tulane University School of Medicine, New Orleans, Louisiana, United States
  • Isakova, Tamara, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States
  • Jaar, Bernard G., Johns Hopkins University and Nephrology Center of Maryland, Baltimore, Maryland, United States
  • Ricardo, Ana C., University of Illinois at Chicago, Chicago, Illinois, United States
  • Hostetter, Thomas H., Case Western Reserve University, Cleveland, Ohio, United States
  • Rahman, Mahboob, Case Western Reserve University, Cleveland, Ohio, United States

Group or Team Name

  • CAC

There is a graded relationship between the severity of chronic kidney disease (CKD) and coronary artery calcification (CAC), though the mechanism is unclear. Metabolic acidosis, a common complication of CKD, contributes to decreased mineral bone content and may lead to worsening vascular calcification. We hypothesize that low serum bicarbonate level, an expression of metabolic acidosis, is a risk factor for CAC in CKD.


Serum bicarbonate and CAC were simultaneously measured in 862 CRIC participants at baseline and after 3 years. CAC was measured using electron beam or multidetector computed tomography and calculated using Agatston score. Serum bicarbonate was analyzed both as a continuous and a categorical variable by the following groups: <22 mEql/L (low), 22-26 mEq/L (normal) and >26 mEq/L (high). CAC progression was defined as follows: CAC> 0 at follow-up, if CAC=0 at baseline; annualized change ≥10 Agatston units at follow-up if 0<CAC≤100 at baseline; and annualized percent change (annualized change in CAC score divided by the baseline CAC score) ≥ 10% at follow-up, if CAC > 100 at baseline. Logistic regression models were built to study the association of interest.


The mean eGFR was 43±17ml/min per 1.73m2, mean serum bicarbonate was 24.4±3.3 mEq/L, and 42.7% participants had diabetes. A total of 412 (48%) participants experienced CAC progression. Participants with low bicarbonate were more likely to have CAC >400 at baseline, and to experience CAC progression, compared to those in the normal group (57.3% vs 46.2%, p=0.003). The low group had 52% higher risk of CAC progression, compared to normal group (OR1.52; 95%CI: 1.02–2.29), in models adjusted for demographics, baseline co-morbidities, medications, calcium and phosphorus. Addition of eGFR and proteinuria to these models attenuated the association (OR 1.34; 95%CI: 0.87–2.08). In fully adjusted models, each 1mEq/L lower serum bicarbonate was associated with 6% higher risk of CAC progression (OR 1.06; 95%CI: 1.01-1.12).


In a cohort of patients with CKD, low serum bicarbonate level was associated with CAC progression. This association may not be independent of kidney function. Further studies are needed to determine a causal link between low serum bicarbonate and CAC.


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