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

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

  • Intensive Care Med Exp. 2024 Jul 8;12(1):64. doi: 10.1186/s40635-024-00647-2.
Abraham H Hulst # 1 2,  Connie P C Ow # 3,  Clive N May 3 4,  Sally H Hood 3,  Mark P Plummer 5,  Jeroen Hermanides 6,  Daniël H van Raalte 7,  Adam M Deane 8,  Rinaldo Bellomo 8 4 9 10,  Yugeesh R Lankadeva 3 4 11
Affiliations

Affiliations

  • 1 Preclinical Critical Care Unit, Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, VIC, Australia. a.h.hulst@amsterdamumc.nl.
  • 2 Department of Anesthesiology, Amsterdam UMC, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands. a.h.hulst@amsterdamumc.nl.
  • 3 Preclinical Critical Care Unit, Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, VIC, Australia.
  • 4 Department of Critical Care, Melbourne Medical School, The University of Melbourne, Melbourne, VIC, Australia.
  • 5 Department of Intensive Care, Royal Adelaide Hospital, Adelaide, Australia.
  • 6 Department of Anesthesiology, Amsterdam UMC, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands.
  • 7 Department of Internal Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands.
  • 8 Department of Intensive Care, Royal Melbourne Hospital, Melbourne, VIC, Australia.
  • 9 Australian and New Zealand Intensive Care Research Centre, Monash University, Melbourne, VIC, Australia.
  • 10 Department of Intensive Care, Austin Hospital, Melbourne, VIC, Australia.
  • 11 Department of Anesthesia, Austin Hospital, Melbourne, VIC, Australia.
  • # Contributed equally.
PMID: 38977627 DOI: 10.1186/s40635-024-00647-2
Abstract

Background: People 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.

Methods: Sixteen 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).

Results: Empagliflozin 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.

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

Keywords

Acute kidney injury; Empagliflozin; Medullary oxygenation; Sepsis; Sodium-glucose transporter 2 inhibitor.

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