Abstract: TH-PO1105
Muscle Injury with Acid Accumulation but Without Metabolic Acidosis in G3 CKD and Its Response to Dietary Acid Reduction: A Five-Year Randomized Trial
Session Information
- CKD: Therapies, Innovations, and Insights
November 06, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: CKD (Non-Dialysis)
- 2302 CKD (Non-Dialysis): Clinical, Outcomes, and Trials
Authors
- Goraya, Nimrit, Baylor Scott and White Central Texas, Temple, Texas, United States
- Simoni, Jan, Texas Tech University System, Lubbock, Texas, United States
- Aksan, Nazan, The University of Texas at Austin Dell Medical School, Austin, Texas, United States
- Kahlon, Maninder, The University of Texas at Austin Dell Medical School, Austin, Texas, United States
- Wesson, Donald E., The University of Texas at Austin Dell Medical School, Austin, Texas, United States
Background
Correction of metabolic acidosis (plasma total CO2 [PTCO2] <22 mM) in study participants with G3-G4 chronic kidney disease (CKD) improved subjectively and objectively assessed physical function (Lancet 394:396, 2019). We tested the hypothesis that participants with G3 CKD and PTCO2 >22 mM but with acid accumulation (AJN 53:794, 2022), for whom current guidelines do not recommend alkali treatment, have muscle injury and dietary acid reduction for five years reduces it.
Methods
Body acid accumulation and serum myosin, a biomarker of muscle injury, were measured cross-sectionally in study participants with G3 [mean (SD) eGFR 39.9 (6.7) ml/min/1.73 m2, n=84] compared to G1 [eGFR 99.2 (7.3) ml/min/1.73 m2, n=62] CKD. Baseline and five-year PTCO2 and serum myosin were measured in 108 separate G3 participants with mean baseline eGFR ~39 ml/min/1.73 m2 randomized to base-producing fruits and vegetables (F&V, n=36) to reduce dietary potential renal acid load by half, oral NaHCO3 (HCO3, n=36) 0.3 mmol/kg bw/day to approximate the F&V base-producing potential, or to Usual Care (UC, n=36). Linear mixed effect regressions were conducted to address these questions.
Results
In cross-sectional studies, G3 vs. G1 acid accumulation [25.6 (9.0) vs. 3.8 (12.5) mmoles, respectively, p<0.05)] and serum myosin [1.35 (0.01) ng/ml vs. 1.09 (0.01), respectively, p<0.01] were higher. In longitudinal studies of G3 participants, five-year vs. baseline PTCO2 was higher in F&V and HCO3 (p<0.05) but was lower in UC (p<0.05) as eGFR declined (p<0.05) in all groups. Five-year vs. baseline serum myosin in G3 was lower in F&V [1.37 (0.02) vs. 1.40 (0.02) ng/ml, respectively, p<0.001] and HCO3 [1.38 (0.02) vs. 1.40 (0.02) ng/ml, p<0.001] but was higher in UC [1.46 (0.02) vs. 1.41 (0.02) ng/ml, p<0.001]. Five-year G3 serum myosin for F&V and HCO3 were higher than UC (p<0.002) but were not different from each other (p=0.94).
Conclusion
The data support that acid accumulation not sufficient to cause metabolic acidosis in participants with G3 CKD caused muscle injury assessed by serum myosin, it increased further as eGFR declined, and dietary acid reduction with NaHCO3 or F&V reduced it. The data support that subclinical acid accumulation in CKD causes muscle injury and warrants treatment with alkali.