Sotagliflozin Helps Manage Anemia in T2D and CKD

TOPLINE:

Sotagliflozin, a dual sodium-glucose cotransporter 1 and 2 inhibitor, rapidly improves hemoglobin levels in patients with type 2 diabetes (T2D) and moderate to severe chronic kidney disease (CKD), regardless of whether anemia is present at baseline.

METHODOLOGY:

• Although erythropoiesis-stimulating agents can boost hemoglobin levels, they also elevate the risk for major cardiovascular events, adding to the challenge of managing anemia in patients with CKD and T2D.
• Researchers conducted a post hoc analysis of pooled data from two clinical trials comparing the effect of sotagliflozin (200 mg and 400 mg) with that of placebo on hemoglobin levels in patients with T2D and CKD stages III-IV who did or did not have anemia.
• Anemia was defined as baseline hemoglobin levels
• The efficacy of sotagliflozin relative to that of placebo in improving hemoglobin levels was evaluated at week 26.

TAKEAWAY:

• Among the 1064 patients analyzed, the mean hemoglobin level at baseline was 12.7 g/dL; 493 patients (46.3%; mean age, 68 years; 46% women) had anemia at baseline.
• Compared with placebo, 200 mg and 400 mg sotagliflozin increased mean hemoglobin levels from baseline to week 26 by 0.39 g/dL and 0.41 g/dL, respectively (P
• The impact of sotagliflozin relative to placebo on hemoglobin levels was similar for patients with and without anemia at baseline (P_interaction = .062).
• Compared with placebo, treatment with sotagliflozin increased mean hemoglobin levels by 0.27 g/dL in participants with anemia and 0.50 g/dL in those without.
• Sotagliflozin significantly increased the likelihood of resolution of anemia over 26 weeks in participants with the condition at baseline (odds ratio, 1.95; P = .017).
• Sotagliflozin was safe and well tolerated among those with and without anemia.

IN PRACTICE:

“Sotagliflozin increased hemoglobin in patients with T2D and CKD, supporting its potential use in the management of anemia in this population, in addition to known cardiorenal protective effects,” the authors wrote.

SOURCE:

The study was led by Vikas S. Sridhar, MD, Toronto General Hospital Research Institute, Toronto, Ontario, Canada. It was published online in Diabetes, Obesity and Metabolism.

LIMITATIONS:

The analyses were exploratory and post hoc in nature. The short follow-up duration limited the ability to assess whether changes in hemoglobin levels with sotagliflozin were sustained or associated with clinically meaningful outcomes. The absence of data on erythropoiesis markers limited the authors’ ability to gain insights into the mechanism by which sotagliflozin impacts hemoglobin.

DISCLOSURES:

The authors declared receiving conference support, honoraria, and operational funding from and being employees or stockholders of various pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.