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Abstract: PO1021

Hemoglobin A1c Reduction with the GLP-1 Receptor Agonist Semaglutide Is independent of Baseline eGFR: Post Hoc Analysis of SUSTAIN and PIONEER Programs

Session Information

Category: Diabetic Kidney Disease

  • 602 Diabetic Kidney Disease: Clinical

Authors

  • Cherney, David, Toronto General Hospital, Toronto, Ontario, Canada
  • Hadjadj, Samy, L'institut du thorax, INSERM CNRS, Univ Nantes, CHU Nantes, Nantes, France
  • Idorn, Thomas, Novo Nordisk A/S, Søborg, Denmark
  • Mosenzon, Ofri, Hadassah Medical Center, Hebrew University of Jerusalem, Jerusalem, Jerusalem, Israel
  • Pilemann-Lyberg, Sascha, Novo Nordisk A/S, Søborg, Denmark
  • Perkovic, Vlado, The George Institute for Global Health, UNSW Sydney, Sydney, New South Wales, Australia
  • Tuttle, Katherine R., Providence Medical Research Center, Providence Health Care, Spokane, Washington, United States
  • Rasmussen, Soren, Novo Nordisk A/S, Søborg, Denmark
  • Bain, Stephen C., Swansea University Medical School, Swansea Univeristy, Swansea, United Kingdom
Background

Hyperglycemia is an established risk factor for the development and progression of chronic kidney disease. The glucagon-like peptide-1 receptor agonist semaglutide is approved for the treatment of type 2 diabetes (T2D) across a wide range of estimated glomerular filtration rates (eGFRs). We investigated whether baseline eGFR affected glycated hemoglobin (HbA1c) reduction with semaglutide.

Methods

This post hoc, trial-level analysis considered all SUSTAIN (1–10) and PIONEER (1–10) trials where renal impairment was not an exclusion criteria and where the number of subjects receiving semaglutide with eGFR <60 mL/min/1.73m2 was >10. It included data for once-weekly subcutaneous semaglutide (SUSTAIN 4–6, pooled 0.5 and 1.0 mg; SUSTAIN 10, 1.0 mg only) and once-daily oral semaglutide (PIONEER 5 and 6, 14 mg); comparator data were not analyzed. Subjects receiving semaglutide were grouped by baseline eGFR; the eGFR subgroups evaluated were selected according to number of subjects meeting eGFR cut-offs (≥60 and <60 mL/min/1.73 m2 in SUSTAIN 4, 5, and 10; <45, 45 to <60 and ≥60 mL/min/1.73 m2 in SUSTAIN 6 and PIONEER 5 and 6). Within each trial, absolute estimated change in HbA1c from baseline to end of treatment (EOT) was compared between eGFR subgroups using a linear mixed model.

Results

Mean HbA1c at baseline ranged from 7.9% to 8.7% across the subgroups. Semaglutide significantly reduced HbA1c at a comparable magnitude across eGFR subgroups in all trials (mean reduction of 1.0–1.7% from baseline to EOT; p>0.148 for difference between eGFR subgroups within each trial; Figure).

Conclusion

Semaglutide (subcutaneous and oral) is an effective glucose-lowering agent in subjects with T2D, independently of baseline eGFR, including in those with chronic kidney disease.

Funding

  • Commercial Support