Abstract: FR-PO0264
Increased Bone Osteoclastic Activity with Acid Accumulation but Without Metabolic Acidosis in G3 CKD and Its Response to Dietary Acid Reduction: A Five-Year Randomized Trial
Session Information
- Bone and Mineral Metabolism: Clinical Epidemiology and Outcomes
November 07, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 502 Bone and Mineral Metabolism: Clinical
Authors
- Goraya, Nimrit, Baylor Scott and White Central Texas, Temple, Texas, United States
- Simoni, Jan, Texas Tech University System, Lubbock, Texas, United States
- Kahlon, Maninder, The University of Texas at Austin Dell Medical School, Austin, Texas, United States
- Aksan, Nazan, 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
Increased osteoclastic resorption of bone releases alkali that buffers accumulating acid of advancing chronic kidney disease (CKD) but also releases mineral that reduces bone health. Current CKD guidelines do not recommend alkali treatment of acid accumulation without metabolic acidosis (i.e., plasma total CO2 [PTCO2] remains >22 mM). We tested the hypothesis that acid accumulation in G3 study paticipants with PTCO2 >22 mM is associated with increased osteoclastic activity that can be reduced with five years of dietary acid reduction.
Methods
Body acid accumulation and 8-hour urine excretion of N-telopeptide (8h-NTX), a biomarker of bone osteoclastic resorption, were measured [mean (SD)] cross-sectionally in G3 [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] study paticipants, all with baseline PTCO2 >22 mM. Baseline and five-year PTCO2 and 8h-NTX were measured longitudinally 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 8h-NTX [147.6 (3.0) vs. 53.9 (4.8) nmol/8h, respectively, p<0.05] were higher. In longitudinal studies, five-year vs. baseline PTCO2 was higher in F&V and HCO3 participants (p<0.05) but was lower in UC (p<0.05) as eGFR declined (p<0.05) in all groups. Five-year vs. baseline 8h NTX in G3 participants was lower in F&V [144.8 (2.8) vs. 146.6 (2.4) nmol/8h, p=0.01], unchanged in HCO3 [146.1 (1.9) vs. 145.3 (2.0) nmol/8h, p=0.64] but was higher in UC [149.9 (2.8) vs. 144.8 (2.7) nmol/8h, p<0.01]. There were no significant 8h-NTX group differences at five years (p=0.15).
Conclusion
The data support that acid accumulation not sufficient to cause metabolic acidosis in G3 CKD increased bone osteoclastic activity, it increased further as eGFR declined, and it can be ameliorated with dietary acid reduction, particularly with F&V.