1831-P: Ertugliflozin Mitigates Blood Pressure Increments during a High-Sodium Diet in People with Type 2 Diabetes

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Introduction and Objective: Individuals with type 2 diabetes (T2D) often experience greater BP increments compared to normoglycemic individuals when consuming a high-sodium diet, a phenomenon referred to as sodium-sensitive hypertension. We hypothesized that the SGLT2i ertugliflozin could mitigate blood pressure increments during a high-sodium (HS) diet in people with T2D. Methods: This randomized, placebo-controlled, 4-arm crossover trial included 34 participants with T2D. They followed HS (250±50 mmol per day) and moderate-sodium (90±18 mmol per day) diets, with compliance verified by 24-h urinary sodium excretion after 7-10 days. Compliant participants then received 10 days of ertugliflozin 15 mg once daily (ERTU) or matching placebo (PLB) in random order, while continuing the diet. At baseline and at the end of each treatment period, 24-h ABPM, 24-h urine samples and blood samples were collected. Here, we analyzed the difference in HS diet-induced BP increment between ERTU and PLB, compared to ABPM measured at screening during a habitual sodium intake (aimed at 150±30 mmol), which was the secondary endpoint of the trial. Participants on RASi or diuretics maintained stable dosages throughout the study. Results: During habitual sodium intake at baseline, participants excreted 132.5 [106.0 - 185.3] mmol urinary sodium per 24 hours with a SBP of 131± 10 mmHg and DBP of 80 ± 7 mmHg. Urinary sodium excretion during HS was similar between PLB (215 ± 81.9 mmol) and ERTU (234 ±77.6 mmol; p=0.203). During PLB treatment, HS diet increased SBP and DBP compared to baseline by 7.2 (SE 1.8) mmHg (p = 0.0002) and 3.5 (SE 1.0) mmHg (p = 0.0015), respectively. During ERTU and HS diet, SBP (+2.1. mmHg, SE 1.8; p=0.240) and DBP (+1.5 mmHg, SE 1.0; p=0.175) did not differ compared to baseline. Thus, ERTU prevented the BP increment induced by HS compared to PLB (SBP: p = 0.007; DBP: p = 0.057). Conclusion: ERTU prevented the BP-increment induced by HS intake without altering sodium excretion. Mitigation of sodium sensitivity by ERTU may contribute to its beneficial cardio-kidney effects. Disclosure B. Wever: None. C.L. Birznieks: None. L. Driscoll: None. J. Kendrick: Advisory Panel; Current; Fresenius Medical Care. Research Support; Current; Eli Lilly and Company, Bayer AG, Novo Nordisk. H. Heerspink: Consultant; Current; AstraZeneca, Alnylam Pharmaceuticals, Inc., Amgen Inc., Bayer AG, Boehringer Ingelheim International GmbH, Dimerix, Eli Lilly and Company, Novo Nordisk, Novartis AG, Roche Pharmaceuticals. P. Bjornstad: Consultant; Current; Bayer AG, Boehringer Ingelheim International GmbH, Lilly, Novo Nordisk. D. van Raalte: Consultant; Current; AstraZeneca. Research Support; Current; AstraZeneca. Consultant; Current; Boehringer Ingelheim International GmbH. Research Support; Current; Boehringer Ingelheim International GmbH. Consultant; Current; Eli Lilly and Company. Research Support; Current; Eli Lilly and Company. Consultant; Current; Merck & Co., Inc. Research Support; Current; Merck & Co., Inc. Consultant; Current; Novo Nordisk. Research Support; Current; Novo Nordisk.

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