ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

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

Authors

  • 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
Background

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.

Methods

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.

Results

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).

Conclusion

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.

Funding

  • Private Foundation Support