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Abstract: SA-PO885

Effects of Dapagliflozin in Patients Without Diabetes and Microalbuminuria: An Exploratory Analysis From the DAPA-CKD Trial

Session Information

Category: CKD (Non-Dialysis)

  • 2202 CKD (Non-Dialysis): Clinical‚ Outcomes‚ and Trials

Authors

  • L Heerspink, Hiddo Jan, Universitair Medisch Centrum Groningen, Groningen, Groningen, Netherlands
  • Chertow, Glenn, Stanford University School of Medicine, Stanford, California, United States
  • Jongs, Niels, Universitair Medisch Centrum Groningen, Groningen, Groningen, Netherlands
  • Correa-Rotter, Ricardo, The National Medical Science and Nutrition Institute Salvador Zubiran, Mexico City, Mexico
  • Rossing, Peter, Steno Diabetes Center Copenhagen, Herlev, Denmark
  • Sjostrom, David, AstraZeneca, Gothenburg, Sweden
  • Langkilde, Anna Maria, AstraZeneca, Gothenburg, Sweden
  • Wheeler, David C., University College London, London, London, United Kingdom

Group or Team Name

  • DAPA-CKD Trial Committee and Investigators
Background

The DAPA-CKD trial demonstrated that the sodium glucose co-transporter 2 inhibitor dapagliflozin slows progressive kidney function loss in patients with CKD without type 2 diabetes. The majority of these participants had macroalbuminuria. Whether this effect persists in participants without type 2 diabetes and with microalbuminuria is unknown. We therefore assessed the effects of dapagliflozin on the rate of kidney function decline, albuminuria, and blood pressure in this subgroup.

Methods

DAPA-CKD randomized participants with or with type 2 diabetes and an urinary albumin-to-creatinine ratio (UACR) 200–5000 mg/g and eGFR 25–75 mL/min/1.73m2 to dapagliflozin 10 mg or placebo once daily, added to standard care. The kidney endpoint was a composite of sustained ≥50% eGFR decline, end-stage kidney disease or renal death. We analyzed, in participants without type 2 diabetes and with microalbuminuria (UACR<300 mg/g), eGFR slope using mixed effect models with slopes from baseline to Week 2 (acute change) and Week 2 to end-of-treatment (chronic eGFR slope). UACR change was an additional pre-specified exploratory outcome.

Results

Of 4304 randomized participants, 136 (72 randomized to dapagliflozin and 64 to placebo) did not have type 2 diabetes and had a UACR <300 mg/g. Their mean age was 61 years, 49 (36%) were female, mean eGFR was 42 mL/min/1.73m2 and median UACR was 245 mg/g. In the dapagliflozin group UACR changed from baseline by -24.2% (95%CI -41.2, -2.3) versus -9.8% (-30.8, 17.7) in the placebo group (between group difference -16.0% [95%CI, -41.8, 21.3]). Compared to placebo, dapagliflozin caused an acute eGFR reduction of 2.4 mL/min/1.73m2 (95%CI 0.4, 4.5). Thereafter, dapagliflozin reduced the mean rate of eGFR decline by 1.8 mL/min/1.73m2 (95%CI 0.4, 3.1) compared to placebo. Few kidney endpoints occurred during follow-up (1 in the dapagliflozin group and 3 in the placebo group).

Conclusion

In patients without type 2 diabetes and with microalbuminuria, dapagliflozin slowed eGFR decline during chronic treatment suggesting that its kidney protective effects may extend to this subgroup of patients.

Funding

  • NIDDK Support