Evidence map›Paper›PMID 38977627›Full record

ArticleIntensive care medicine experimental2024

Effects of sodium-glucose transporter-2 inhibition on systemic hemodynamics, renal function, and intra-renal oxygenation in sepsis-associated acute kidney injury.

Abraham H Hulst, Connie P C Ow, Clive N May, Sally H Hood, Mark P Plummer, Jeroen Hermanides, Daniël H van Raalte, Adam M Deane, Rinaldo Bellomo, Yugeesh R Lankadeva

Abstract read
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In one paragraph

Article in Intensive care medicine experimental, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

10 authors.

Abraham H Hulst *Preclinical Critical Care Unit, Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, VIC, Australia. a.h.hulst@amsterdamumc.nl.ORCID http://orcid.org/0000-0001-9101-7649
Connie P C Ow *Preclinical Critical Care Unit, Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, VIC, Australia.
Clive N MayPreclinical Critical Care Unit, Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, VIC, Australia.
Sally H HoodPreclinical Critical Care Unit, Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, VIC, Australia.
Mark P PlummerDepartment of Intensive Care, Royal Adelaide Hospital, Adelaide, Australia.
Jeroen HermanidesDepartment of Anesthesiology, Amsterdam UMC, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands.
Daniël H van RaalteDepartment of Internal Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands.
Adam M DeaneDepartment of Intensive Care, Royal Melbourne Hospital, Melbourne, VIC, Australia.
Rinaldo BellomoDepartment of Intensive Care, Royal Melbourne Hospital, Melbourne, VIC, Australia.
Yugeesh R LankadevaPreclinical Critical Care Unit, Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, VIC, Australia.

Funding

Centre of Excellence in Cognition and its Disorders, Australian Research Council GNT2025266H2020 European Research Council 101024833National Heart Foundation of Australia FLF105666ZonMw 452020104
6 · The paper itself

Abstract

backgroundPeople with type 2 diabetes mellitus treated with sodium-glucose transporter-2 inhibitors (SGLT2i) have lower rates of acute kidney injury (AKI). Sepsis is responsible for the majority of AKI in critically ill patients. This study investigated whether SGLT2i is renoprotective in an ovine model of Gram-negative septic AKI.

methodsSixteen healthy merino ewes were surgically instrumented to enable measurement of mean arterial pressure, cardiac output, renal blood flow, renal cortical and medullary perfusion, and oxygenation. After a 5-day recovery period, sepsis was induced via slow and continuous intravenous infusion of live Escherichia coli. Twenty-three hours later, sheep were randomized to receive an intravenous bolus of 0.2 mg/kg empagliflozin (n = 8) or a fluid-matched vehicle (n = 8).

resultsEmpagliflozin treatment did not significantly reduce renal medullary hypoperfusion or hypoxia, improve kidney function, or induce histological changes. Renal cortical oxygenation during the intervention period was 47.6 ± 5.9 mmHg in the empagliflozin group compared with 40.6 ± 8.2 mmHg in the placebo group (P = 0.16). Renal medullary oxygenation was 28.0 ± 18.5 mmHg in the empagliflozin compared with 25.7 ± 16.3 mmHg (P = 0.82). Empagliflozin treatment did not result in significant between-group differences in renal blood flow, kidney function, or renal histopathological changes.

conclusionIn a large mammalian model of septic AKI, a single dose of empagliflozin did not improve renal microcirculatory perfusion, oxygenation, kidney function, or histopathology.

Indexed as

Acute kidney injuryEmpagliflozinMedullary oxygenationSepsisSodium-glucose transporter 2 inhibitor

Identifiers

PMID38977627
PMCPMC11231125

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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 OpenQuestion graph.