Kidney Week

Abstract: TH-OR025

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

Session Information

• CKD-MBD: Phosphorus, FGF-23, and Trials
  October 25, 2018 | Location: 33C, San Diego Convention Center
  Abstract Time: 05:18 PM - 05:30 PM

Category: Bone and Mineral Metabolism

• 402 Bone and Mineral Metabolism: Clinical

Authors

• Dobre, Mirela A., Case Western Reserve University, Cleveland, Ohio, United States

Mirela A. Dobre, MD

• Patel, Neil H., Case Western Reserve University, Cleveland, Ohio, United States

Neil H. Patel,

• Yang, Wei, University of Pennsylvania, Philadelphia, Pennsylvania, United States

Wei Yang,

• Chen, Jing, Tulane School of Medicine, New Orleans, Louisiana, United States

Jing Chen,

• Hamm, L. Lee, Tulane University School of Medicine, New Orleans, Louisiana, United States

L. Lee Hamm,

• Isakova, Tamara, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States

Tamara Isakova,

• Jaar, Bernard G., Johns Hopkins University and Nephrology Center of Maryland, Baltimore, Maryland, United States

Bernard G. Jaar,

• Ricardo, Ana C., University of Illinois at Chicago, Chicago, Illinois, United States

Ana C. Ricardo,

• Hostetter, Thomas H., Case Western Reserve University, Cleveland, Ohio, United States

Thomas H. Hostetter,

• Rahman, Mahboob, Case Western Reserve University, Cleveland, Ohio, United States

Mahboob Rahman,

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