Abstract: TH-PO0013
Pilot Study to Assess Feasibility of the Therapeutic Use of Malic Acid for Hypocitraturia
Session Information
- Mineral Balance: Physiology and Pathophysiology
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 501 Bone and Mineral Metabolism: Basic
Authors
- Gianella, Fabiola, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Lederer, Eleanor D., VA North Texas Health Care System, Dallas, Texas, United States
Background
Low urinary citrate (Cit) is a risk factor for nephrolithiasis. Standard therapy with potassium Cit is effective but limited by poor tolerance, variable response, and excessive increases in urine pH. Prior studies suggested that oral malic acid effectively increased urine Cit but the mechanism was not determined. We hypothesized that the tricarboxylic acid malic acid would increase urine Cit by competing with filtered Cit for proximal tubule reabsorption.
Methods
We recruited 10 healthy normocitraturic volunteers to conduct a pilot three-phase study: 1 week baseline, 1 week supplemental L-malic acid, and 1 week recovery on a metabolic diet( 75 gr prot, 275 gr cho, 68 g fat, 2300mg Na+,1959mg k+, 800 mg Pi, 400 mg Ca++.) 5 participants received 600 mg twice daily pure L-malic acid and 5 subjects received 1.6 twice daily during the treatment week. At the end of each phase, spot serum malate, citrate, and creatinine were measured. 2-24h urine samples for malate, citrate, and creatinine were obtained. The data were analyzed by Wilcoxon signed rank test (median (IQR) baseline vs treatment phase).
Results
The subjects were 80% female, 100% white, 50% Hispanic. Mean age was 37.5 ±10y. Pure oral L-malic acid was well tolerated at both doses. Malic acid produced a minimal nonsignificant increase in serum malate (µM) levels baseline vs treatment 2.4(2.2-2.6) vs 2.6 (2.2-2.8), p=0.4 in the low dose group and 2.28 (2.1-3.1) vs 2.34 (2.21-2.61), p=1 in the high dose group, and no significant change in urinary malate (mg/day), 2.83(2.39-3.83) vs 2,66 (2.48-2.88), p=0.63(low dose), 1.65 (1.31-4.02) vs 2.17 (1.62-2.33), p=0.81 (high dose). Serum Cit (µM) levels were nonsignificant as well, 116 (102-120) vs 115 (101-120), p=0.38 (low dose), 113 (102-114) vs 118 (108-119) p=0.19 (high dose). Urinary Cit (mg/day) varied widely at baseline with no significant increase from baseline level vs treatment, 692 (459-813) vs 737 (505-752), p=0.81 (low dose), 642.8(359-986) vs 586.7 (318-995) p=0.81 (high dose). Urine pH was not significantly affected.
Conclusion
The failure of pure oral malic acid to increase citraturia suggests that only the salt form of the tricarboxylic acids increases citraturia, likely by an alkalinizing effect.
Funding
- Private Foundation Support