Abstract: TH-PO0393
Effect of Sodium Bicarbonate on Serum Calciprotein Particles in CKD
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 1
November 06, 2025 | 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
- Eiwaz, Mahaba B, Albert Einstein College of Medicine, New York, New York, United States
- Koike, Seiji, Oregon Health & Science University, Portland, Oregon, United States
- Graham, Garry Anthony, Albert Einstein College of Medicine, New York, New York, United States
- Dobre, Mirela A., Case Western Reserve University, Cleveland, Ohio, United States
- Lapidus, Jodi A., Oregon Health & Science University, Portland, Oregon, United States
- Abramowitz, Matthew K., Albert Einstein College of Medicine, New York, New York, United States
- Hostetter, Thomas H., The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina, United States
- Cheung, Alfred K., University of Utah Health, Salt Lake City, Utah, United States
- Raphael, Kalani L., University of Utah Health, Salt Lake City, Utah, United States
- Melamed, Michal L., NYU Langone Health, New York, New York, United States
- Chen, Wei, Albert Einstein College of Medicine, New York, New York, United States
Background
Animal studies suggest that sodium bicarbonate may worsen vascular calcification. A faster transformation (i.e., low T50) from primary to secondary calciprotein particles (CPP2) and/or larger CPP2 suggest a reduced mineral buffering capacity in blood and is associated with mortality. Here, we tested the hypothesis that sodium bicarbonate reduces T50 and increases CPP2 size in blood.
Methods
We performed post hoc analyses of two published double-blind, placebo-controlled trials of oral sodium bicarbonate therapy in CKD: the VA-Bicarb Trial (n=74) and Alkali Therapy in CKD Trial (n=149). Participants with normal serum bicarbonate levels were randomized to receive either sodium bicarbonate 0.4-0.5 mEq/kg/day or placebo. In the stored serum samples obtained from baseline, month 3 and month 6, we measured 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 size in each trial and pooled data.
Results
In VA Bicarb Trial, eGFR was 52±18mL/min/1.73m2 at baseline; T50 was 154 ± 44 min. There was no significant change in T50 with sodium bicarbonate therapy (Figure). In Alkali Therapy in CKD Trial, eGFR was 36±11mL/min/1.73m2 at baseline; T50 was 131 ± 36 min. At month 3, the mean T50 was 14 minutes higher (95% CI, 1-26, p=0.03) in bicarbonate treated patients relative to placebo, while there was no significant change in T50 at month 6. In pooled analyses of both trials, the mean T50 was 12 minutes higher (95% CI, 2-22, p=0.02) in the bicarbonate group relative to placebo at month 3, while there was no significant change in T50 at month 6. There was no significant change in CPP2 size in either trial or in pooled analyses.
Conclusion
In people with CKD, T50 increased after 3 months of oral sodium bicarbonate therapy but this effect was not sustained after 6 months. Notably, the effect was primarily observed in the Alkali Therapy in CKD Trial, in which participants had lower eGFR, suggesting that any positive effect may be observed in those with worse kidney function.
Funding
- NIDDK Support