ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

ASN / Education & Meetings / Kidney Week /

Please note that you are viewing an archived section from 2020 and some content may be unavailable. To unlock all content for 2020, please visit the archives.

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 –