Kidney Week

Abstract: SA-PO494

Effect of Sodium Bicarbonate Therapy on Calciprotein Particles in Patients with CKD Stages 3 and 4 and Mild Metabolic Acidosis

Session Information

• Acid-Base, Calcium, Potassium, and Magnesium Disorders: Clinical
  October 26, 2024 | Location: Exhibit Hall, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Fluid, Electrolytes, and Acid-Base Disorders

• 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

• Chen, Wei, Albert Einstein College of Medicine, Bronx, New York, United States

Wei Chen, MD, MS, FASN

• Dobre, Mirela A., University Hospitals, Cleveland, Ohio, United States

Mirela A. Dobre, MD, FASN, MPH

• Koike, Seiji, Oregon Health & Science University, Portland, Oregon, United States

Seiji Koike, MS

• Lapidus, Jodi A., Oregon Health & Science University, Portland, Oregon, United States

Jodi A. Lapidus, PhD

• Graham, Garry Anthony, Albert Einstein College of Medicine, Bronx, New York, United States

Garry Anthony Graham

• Abramowitz, Matthew K., Albert Einstein College of Medicine, Bronx, New York, United States

Matthew K. Abramowitz, MD, MS, FASN

• Hostetter, Thomas H., The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina, United States

Thomas H. Hostetter, MD

• Cheung, Alfred K., University of Utah Health, Salt Lake City, Utah, United States

Alfred K. Cheung, MD

• Raphael, Kalani L., University of Utah Health, Salt Lake City, Utah, United States

Kalani L. Raphael, MD, MS, FASN

• Melamed, Michal L., NYU Langone Health, New York, New York, United States

Michal L. Melamed, MD

Background

Animal studies suggest that sodium bicarbonate, used to treat metabolic acidosis of CKD, may worsen vascular calcification. Calciprotein particles (CPPs) are nanoparticles of calcium phosphate crystals and calcification inhibitors. Faster transformation (i.e., low T₅₀) from primary to secondary CPP (CPP2) and larger CPP2 indicate a reduced mineral buffering capacity in blood and are associated with mortality. In people with CKD, we tested the hypothesis that sodium bicarbonate therapy reduces T₅₀ and increases CPP2 size.

Methods

We performed secondary analyses of a double-blind, placebo-controlled trial, in which 149 participants with CKD stage 3 or 4 with serum bicarbonate levels 22-26 mEq/L were randomized to receive either sodium bicarbonate 0.4 mEq/kg/day or placebo. In the stored serum samples at baseline, month 2 and 6, we measured the time for half maximal CPP transformation (T₅₀) using nephelometry and CPP2 size using dynamic light scattering. Linear mixed effect models were used to test the effects of sodium bicarbonate on the changes in T₅₀ and CPP2.

Results

54% were women and 58% were Black. At baseline, mean (±SD) age was 62±10 years; serum bicarbonate was 24.0±2.2 mEq/L; eGFR was 36±11mL/min/1.73m²; T₅₀ was 131±36 min; and CPP2 was 193±49 nm. At Month 2, serum bicarbonate in the intervention group increased to 26.4 mEq/L and T₅₀ increased by 10 min. These changes were significantly higher than placebo (p<0.001 and p=0.03, respectively). At Month 6, mean serum bicarbonate was 25.5 mEq/L and there was no change in T₅₀ compared to placebo. There was no significant change in CPP2 at either Month 2 or 6.

Conclusion

In contrary to our hypothesis, oral sodium bicarbonate therapy in people with CKD increased T₅₀ after 2 months, suggesting improved mineralization capacity; however, this effect was not sustained at 6-month follow-up. Further studies are required to confirm these findings and to investigate whether this increase in T₅₀ improves vascular calcification and survival.

Funding

• NIDDK Support