Abstract: TH-PO0091
Association of Hypercitraturia with Acid Load Markers in Patients with Kidney Stones
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical Research
October 22, 2026 | Location: Exhibit Hall A, 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
- Nayak, Apurva, The University of Chicago, Chicago, Illinois, United States
- Froehlig, Sigrid, The University of Chicago, Chicago, Illinois, United States
- Prochaska, Megan, The University of Chicago, Chicago, Illinois, United States
Background
Urinary anions are hypothesized to originate from both anions that exit cells after metabolism into the blood or through diet as absorbed alkali. Urinary citrate is a dietary anion and an inhibitor of kidney stone formation. We hypothesize that hypercitraturia is reflective of a loss of cell citric acid into the blood, and therefore, is an acid load, rather than reflecting an alkali load from diet. By analyzing changes in various acid load markers, we can provide evidence for either the cellular or dietary origin of hypercitraturia.
Methods
We used pretreatment datasets from Litholink and our Kidney Stone Prevention Clinic containing matched 24-hour urine collections and serum samples. Low, medium, and high tertiles were created based on urinary citrate, within sex. Based on these tertiles, ANOVA tests were performed within sex, on demographic, urine and serum parameters. We used adjusted and unadjusted stratified linear regression models to determine the association between urinary citrate and markers of acid handling, urine ammonia, serum bicarbonate, urine pH, urine phosphorus, titratable acidity (TA), and net acid excretion (NAE). Models were adjusted for sex, weight, age, and GI anion.
Results
In the high citrate tertile, urine ammonia rose, serum bicarbonate fell, urine pH fell, TA rose, and NAE rose. In the low citrate tertile, we observed the opposite; urine ammonia fell, serum bicarbonate rose, and NAE fell. There was variability between datasets for urine pH and TA in the lowest tertile. These findings are corroborated by the figures depicting the association of urinary citrate with each acid load marker.
Conclusion
In the low tertile, citrate acts as an alkali, correlating with lower urine ammonia and higher serum bicarbonate. However, in the high tertile, citrate appears to act as an acid, associated with higher urine ammonia and lower serum bicarbonate. Presumably, it is present as citric acid, acting as a proton donor for extracellular fluid buffers, supporting our hypothesis that its source is cellular metabolism.