Does dapagliflozin (SGLT2 inhibitor) lower uric acid levels?

Medical Advisory BoardAll articles are reviewed for accuracy by our Medical Advisory Board
Educational purpose only • Exercise caution as content is pending human review
Article Review Status
Submitted
Under Review
Approved

Last updated: November 6, 2025View editorial policy

Personalize

Help us tailor your experience

Which best describes you? Your choice helps us use language that's most understandable for you.

Does Dapagliflozin Lower Uric Acid?

Yes, dapagliflozin consistently lowers serum uric acid levels by increasing urinary uric acid excretion through mechanisms linked to urinary glucose excretion. 1, 2, 3

Mechanism of Uric Acid Reduction

Dapagliflozin reduces serum uric acid through increased renal excretion rather than decreased production:

  • Fractional uric acid excretion increases significantly when dapagliflozin is administered, with studies showing increases from 0.9% to 2.9% (P=0.035) after just one week of treatment 3

  • The uric acid-lowering effect correlates strongly with urinary glucose excretion (r=0.35; P=0.02), suggesting the mechanism involves competition at renal tubular transporters 1

  • Urate transporter 1 (URAT1) appears to be involved in this process, as the uric acid-lowering effect of empagliflozin (another SGLT2 inhibitor) is attenuated when combined with benzbromarone, a URAT1 blocker 1

Magnitude and Timeline of Effect

The uric acid reduction with dapagliflozin is clinically meaningful and occurs rapidly:

  • Serum uric acid decreases by approximately 0.8-1.2 mg/dL across multiple studies 1, 2, 3

  • Effects are evident within one week of initiating therapy, with serum uric acid dropping from 347.75 μmol/L to 273.25 μmol/L (P=0.001) 3

  • After 3 months of treatment, serum uric acid levels decreased from 9.0 to 8.0 mg/dL, while urinary uric acid percentage increased from 16.1% to 23.6% 2

  • The effect persists across different metabolic states, including fasting, hyperinsulinemic-euglycemic, and hyperglycemic conditions 1

Clinical Context and Comparative Data

When comparing dapagliflozin to other diabetes medications:

  • SGLT2 inhibitors (dapagliflozin and empagliflozin) significantly outperform traditional oral antihyperglycemic drugs in reducing serum uric acid, with mean levels dropping from 7.5±2.5 to 6.3±0.8 mg/dL versus 7.1±1.8 to 6.8±2.2 mg/dL in the comparator group (p=0.001) 4

  • The uric acid-lowering effect occurs independently of glycemic control improvement, though both effects are observed simultaneously 2, 3

  • Early evidence from 2010 already identified decreased serum uric acid as a beneficial effect of dapagliflozin treatment 5

Important Clinical Considerations

The uric acid-lowering effect is consistent but should not be the primary indication for prescribing dapagliflozin, as the drug is indicated for diabetes management, heart failure, and chronic kidney disease based on major cardiovascular and renal outcome trials 6, 7

This effect may contribute to the renoprotective benefits observed in large outcome trials, as hyperuricemia is associated with cardiovascular and renal complications in diabetes 4

The mechanism differs from traditional uric acid-lowering agents like allopurinol (which inhibits production) or probenecid (which blocks reabsorption), as dapagliflozin's effect is mediated through increased glucose-dependent uric acid excretion 1

References

Research

SGLT2 Inhibition and Uric Acid Excretion in Patients with Type 2 Diabetes and Normal Kidney Function.

Clinical journal of the American Society of Nephrology : CJASN, 2022

Research

Dapagliflozin: more than just another oral glucose-lowering agent?

Expert opinion on investigational drugs, 2010

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Guideline

Dapagliflozin in Chronic Kidney Disease Management

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

Have a follow-up question?

Our Medical A.I. is used by practicing medical doctors at top research institutions around the world. Ask any follow up question and get world-class guideline-backed answers instantly.