Evidence map›Paper›PMID 40444388›Full record

Trial reportDiabetes, obesity & metabolism2025

Effects of dapagliflozin on sodium excretion, blood pressure and volume status in patients with type 2 diabetes and/or chronic kidney disease: The DAPASALT trial.

Jelle M Beernink, Niels Jongs, Charlotte M Mosterd, Rosalie A Scholtes, Alyssa Caldwell-McGee, Daniel Casillas, Lynette Driscoll, Peter J Greasley, Cecilia Karlsson, Ann Hammarstedt and 7 more

Abstract readClinical Trial, Phase IVMulticenter Study
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Diabetes, obesity & metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Trial
  2. Trial
  3. Trial
  4. Salt and chronic kidney disease.Nature reviews. Nephrology · 2026
    Review
  5. Review
  6. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors.

Jelle M BeerninkDepartment of Clinical Pharmacy and Pharmacology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.ORCID https://orcid.org/0000-0002-4615-9012
Niels JongsDepartment of Clinical Pharmacy and Pharmacology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Charlotte M MosterdDepartment of Endocrinology and Metabolism, Amsterdam University Medical Centers, Location VUMC, Diabetes Center, Amsterdam, The Netherlands.
Rosalie A ScholtesDepartment of Endocrinology and Metabolism, Amsterdam University Medical Centers, Location VUMC, Diabetes Center, Amsterdam, The Netherlands.
Alyssa Caldwell-McGeeDivision of Renal Diseases and Hypertension, Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado, USA.
Daniel CasillasDivision of Renal Diseases and Hypertension, Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado, USA.
Lynette DriscollDivision of Renal Diseases and Hypertension, Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado, USA.
Peter J GreasleyResearch and Early Development, Cardiovascular, Renal and Metabolism, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Mölndal, Sweden.
Cecilia KarlssonLate-Stage Development, Cardiovascular, Renal and Metabolism, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden.
Ann HammarstedtLate-Stage Development, Cardiovascular, Renal and Metabolism, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden.
Vikas S SridharDepartment of Medicine, Division of Nephrology, University Health Network, University of Toronto, Toronto, Ontario, Canada.ORCID https://orcid.org/0000-0001-7947-1822
Marcel H A MuskietDepartment of Endocrinology and Metabolism, Amsterdam University Medical Centers, Location VUMC, Diabetes Center, Amsterdam, The Netherlands.
Gozewijn D LavermanDepartment of Internal Medicine, ZGT Hospital, Almelo and Hengelo, The Netherlands.
David Z I CherneyDepartment of Medicine, Division of Nephrology, University Health Network, University of Toronto, Toronto, Ontario, Canada.ORCID https://orcid.org/0000-0003-4164-0429
Petter BjornstadDivision of Metabolism, Endocrinology and Metabolism, Department of Medicine, University of Washington, Seattle, Washington, USA.
Daniel H van RaalteDepartment of Endocrinology and Metabolism, Amsterdam University Medical Centers, Location VUMC, Diabetes Center, Amsterdam, The Netherlands.
Hiddo J L HeerspinkDepartment of Clinical Pharmacy and Pharmacology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.ORCID https://orcid.org/0000-0002-3126-3730

Funding

AstraZeneca Mölndal
6 · The paper itself

Abstract

aimsWe assessed the effects of dapagliflozin on natriuresis and blood pressure in patients with type 2 diabetes and chronic kidney disease (CKD) and evaluated the consistency of these effects across patients with type 2 diabetes without CKD and CKD without type 2 diabetes. MATERIALS AND

methodsWe conducted a mechanistic, nonrandomised, open-label study to evaluate the effects of dapagliflozin on sodium excretion and blood pressure in patients with type 2 diabetes and CKD under a standardised sodium intake (150 mmol/day). Evaluations were performed at baseline (average of Days -3 to -1), treatment start (average of Days 2-4; hereafter referred to as Day 4), treatment end (average of Days 12-14; hereafter referred to as Day 14) and washout (average of Days 15-17). Similar protocols were applied to the type 2 diabetes without CKD and CKD without type 2 diabetes strata. Data from all strata were pooled to assess the consistency of the effects of dapagliflozin.

resultsIn 13 participants with type 2 diabetes and CKD, 24-h sodium excretion did not increase during treatment, as reflected by changes from baseline (Day 4 change: -0.5 mmol/24-h [95% CI -15.4, 14.5], p = 0.95; Day 14 change: -11.7 mmol/24-h [95% CI -30.4, 7.1]). Compared to baseline, 24-h systolic blood pressure decreased by 6.0 mmHg [95% CI -19.8, 7.7] at Day 4 and by 3.7 mmHg [95% CI -13.7, 6.2] at Day 14. In the pooled stratum of 33 participants, 24-h sodium excretion remained unchanged relative to baseline (Day 4 change: -7.4 mmol/24-h [95% CI -16.2, 1.5], p = 0.10; Day 14 change: -10.1 mmol/24-h [95% CI -25.1, 5.0], p = 0.18), whereas 24-h systolic blood pressure was consistently reduced by 6.8 mmHg ([95% CI -10.4, -3.3], p < 0.001) at Day 4 and by 6.5 mmHg ([95% CI -10.1, -3.0], p < 0.001) at Day 14, with no evidence of heterogeneity across strata.

conclusionsDapagliflozin reduced blood pressure during standardised sodium intake in patients with type 2 diabetes and/or CKD without increasing sodium excretion, suggesting that the blood pressure-lowering effects occur through mechanisms beyond natriuresis.

Indexed as

Blood PressureDiabetes Mellitus, Type 2Diabetic NephropathiesNatriuresisRenal Insufficiency, ChronicSodium-Glucose Transporter 2 InhibitorsAgedBenzhydryl CompoundsFemaleGlucosidesHumansMaleMiddle AgedSodiumBenzhydryl CompoundsdapagliflozinGlucosidesSodiumSodium-Glucose Transporter 2 Inhibitorsclinical trialdapagliflozindrug mechanismSGLT2 inhibitortype 2 diabetes

Identifiers

PMID40444388
PMCPMC12232338

What Socratic holds

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LicenceCC BY-NC
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.