Abstract: PO0410
Proton-Pump Inhibitors Are Associated with Decreased Urinary Citrate Excretion
Session Information
- Calcified Tissues in Kidney Diseases
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 402 Bone and Mineral Metabolism: Clinical
Authors
- Patel, Parth M., Loyola University Health System, Maywood, Illinois, United States
- Kandabarow, Alexander, Loyola University Health System, Maywood, Illinois, United States
- Aiwerioghene, Eseosa, Loyola University Health System, Maywood, Illinois, United States
- Blanco-Martinez, Enrique, Loyola University Health System, Maywood, Illinois, United States
- Hart, Spencer, Loyola University Health System, Maywood, Illinois, United States
- Leehey, David J., Loyola University Health System, Maywood, Illinois, United States
- Farooq, Ahmer, Loyola University Health System, Maywood, Illinois, United States
- Baldea, Kristin, Loyola University Health System, Maywood, Illinois, United States
- Turk, Thomas, Loyola University Health System, Maywood, Illinois, United States
Background
Proton-pump inhibitors (PPIs) may increase the risk of kidney stone formation, but the mechanism(s) has not been elucidated. PPI-associated hypomagnesemia is due to impaired intestinal magnesium absorption thought to result from changes in intestinal pH that decrease binding of magnesium to its transporters. Citrate is a tricarboxylic acid with pKa values of 2.9, 4.8, and 5.6. Since citrate is transported primarily in the divalent form (citrate2-) by the intestinal sodium dicarboxylate transporter (NaDC1), changes in intestinal pH by PPIs might decrease the amount of the divalent form, thus reducing intestinal absorption of citrate, thereby decreasing alkaline load and urinary citrate excretion.
Methods
We performed a retrospective review of nephrolithiasis patients treated at our institution and compared patients who were taking PPIs or not at the time of their 24-hour urine collections. Hierarchical multivariate linear regression was used to evaluate the independent relationship between PPI use and urinary composition.
Results
We identified 301 consecutive patients, 88 (29%) of whom were taking PPIs at the time of their 24-hour urine collections. Patients taking PPIs were older and more likely to have medical comorbidities associated with metabolic syndrome such as hypertension, diabetes, and dyslipidemia (p<0.01). Controlling for these factors, patients taking PPIs were found to have lower 24-hour urine citrate excretion (β=-0.12, ΔF=4.24, p=0.04). 24-hour urine magnesium excretion was numerically but not significantly lower in patients taking PPIs. There were no other differences in urinary composition between the groups.
Conclusion
Our findings suggest that patients who take PPIs regularly may be at risk for decreased urinary citrate excretion, which is a known risk factor for kidney stone formation. It is possible that the decrease in urinary citrate with PPIs may have clinical significance, particularly in patients with idiopathic hypocalciuria or other conditions associated with hypocitraturia such as genetic polymorphisms of the renal sodium-citrate transporter, chronic metabolic acidosis, use of carbonic anhydrase inhibitors, high animal protein diet intake, and incomplete distal RTA.