Baseline Sodium-Glucose Cotransporter-2 Inhibitor Use Strongly Attenuates the Uric Acid-Elevating Effect of Thiazide Exposure

Alper Tuna Güven; Murat Özdede; Yusuf Ziya Şener

doi:10.58600/eurjther1889

Authors

Alper Tuna Güven Department of Internal Medicine, Division of General Internal Medicine, Faculty of Medicine, Başkent University, Ankara, Turkey https://orcid.org/0000-0002-6310-4240
Murat Özdede Department of Internal Medicine, Division of General Internal Medicine, Faculty of Medicine, Hacettepe University, Ankara, Turkey https://orcid.org/0000-0002-6981-1210
Yusuf Ziya Şener Department of Internal Medicine, Faculty of Medicine, Hacettepe University, Ankara, Turkey https://orcid.org/0000-0001-5151-5133

DOI:

https://doi.org/10.58600/eurjther1889

Keywords:

Sodium glucose cotransporter 2 inhibitors, hypertension, uric acid, thiazides

Abstract

Objective: Thiazide diuretics are among the major anti-hypertensive medications. However, their hyperuricemic effect restricts their use in patients with gout. Sodium glucose co-transporter 2 inhibitor (SGLT-2i) initiation lowers serum uric acid (SUA) levels. It is not known whether existing SGLT-2i use affects the SUA increasing effect of thiazides.

Methods: Post-hoc data analysis of our published study was conducted. Hypertensive patients who were initiated on thiazide diuretics or whose dose escalated were included (thiazide exposure). Demographic, clinical, and laboratory data were acquired via an electronic database. Patients were grouped according to SGLT-2i presence at the time of thiazide exposure. Since the number of SGLT-2i users was low, bootstrapping via simple random sampling was performed.

Results: 144 patients were included in the study, of whom 13 were on SGLT-2i. Initial sample analysis revealed that while baseline SUA levels were similar between groups, SUA change was significantly lower after thiazide exposure among patients receiving SGLT-2i (0.6 vs. 0.2, p = 0.039). Similarly, baseline SUA levels were similar, but SUA change after thiazide exposure was significantly lower among patients receiving SGLT-2 on bootstrapped data (0.13 [-0.25 - 0.57, 95%CI], vs. 0.61 [0.45 - 0.78, 95%CI], mean difference = 0.48, [0.04 - 0.91, 95%CI], p = 0.029).

Conclusion: This study revealed that thiazide diuretics may be a safe anti-hypertensive medication in terms of hyperuricemia among patients using SGLT-2i. Further studies with similar outcomes may result in the elimination of restrictive recommendations for the use of thiazides in patients with hyperuricemia or gout, provided patients are on SGLT-2i.

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