Related Experiment Video

Updated: Jan 23, 2026

Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion
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Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion

Published on: June 15, 2019

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Sodium glucose transporter 2 inhibition maintains kidney antibacterial response by decreasing complement C1q

Georg W Sendtner1, Julia Miranda1, Pia Naumann1

  • 1Nephrology Section, Medical Clinic 1, University Hospital Bonn, Rheinische Friedrich-Wilhelms Universität, Bonn, Germany.

Kidney International
|January 21, 2026
PubMed
Abstract

Insights

Sodium-glucose transporter 2 inhibition (SGLT2i) surprisingly does not increase urinary tract infection (UTI) risk in kidney disease. SGLT2i regulates complement C1q, enhancing monocyte antibacterial functions and potentially protecting kidneys.

Area of Science:

  • Nephrology
  • Immunology
  • Microbiology

Background:

  • Glucose fuels bacterial growth, yet SGLT2 inhibitors (SGLT2i) used in kidney disease don't raise UTI rates.
  • Investigating the mechanisms behind this unexpected finding is crucial for patient care.

Purpose of the Study:

  • To elucidate the mechanisms by which SGLT2 inhibition impacts kidney bacterial infection response.
  • To explore the role of complement C1q in this process.

Main Methods:

  • Utilized a mouse model of pyelonephritis and human cell cultures.
  • Employed histology, flow cytometry, and gene expression analysis.
  • Examined SGLT2 inhibition's effects on urinary glucose, C1q, and myeloid cell markers.

Main Results:

  • SGLT2i treatment sustained kidney antibacterial response in pyelonephritis models.
  • Decreased complement C1q expression and serum levels were observed with SGLT2i.
  • SGLT2i modulated C1q and MERTK on myeloid cells, impacting monocyte antibacterial functions.

Conclusions:

  • SGLT2i regulates C1q and monocyte antibacterial functions, explaining the lack of increased UTI risk.
  • Complement C1q may be a pathogenic factor in chronic kidney damage and warrants further investigation for SGLT2i therapy.
Keywords:
C1q complementSGLT2 inhibitionpyelonephritis

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