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Updated: Apr 24, 2026

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
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Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice

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Uncoupling glucosuria from infection: SGLT2 inhibition modulates kidney immune response during pyelonephritis

Laura Schwartz1, John David Spencer1

  • 1Kidney and Urinary Tract Center, Nationwide Children's Hospital, Columbus, Ohio, USA; The Ohio State University College of Medicine, Department of Pediatrics, Columbus, Ohio, USA.

Kidney International
|April 22, 2026
PubMed

Insights

Sodium-glucose cotransporter 2 inhibitors like empagliflozin may not increase severe urinary tract infection risk. Research suggests empagliflozin preserves kidney antibacterial defenses, offering a potential explanation for this clinical observation.

Area of Science:

  • Nephrology
  • Infectious Diseases
  • Pharmacology

Background:

  • Sodium-glucose cotransporter 2 (SGLT2) inhibitors increase urinary glucose, theoretically raising urinary tract infection (UTI) risk.
  • Clinical trials show SGLT2 inhibitors do not increase severe UTI rates, creating a therapeutic paradox.

Purpose of the Study:

  • To investigate the mechanistic basis for the observed lack of increased severe UTI risk with SGLT2 inhibition.
  • To explore the effects of empagliflozin on kidney antibacterial defenses and inflammatory responses.

Main Methods:

  • Analysis of human cohort data.
  • Experimental pyelonephritis model in mice.
  • Assessment of C1q expression, inflammatory signaling, and antibacterial defenses.

Main Results:

  • Empagliflozin treatment was associated with reduced C1q expression in the kidney.
  • SGLT2 inhibition preserved key antibacterial defense mechanisms.
  • Altered inflammatory signaling pathways were observed in response to empagliflozin.

Conclusions:

  • SGLT2 inhibition with empagliflozin may modulate kidney antibacterial defenses.
  • These mechanisms could explain the absence of increased severe UTI risk despite increased urinary glucose.
  • Empagliflozin may offer a protective effect on kidney infection defense pathways.

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