Deciphering the kidney hemodynamic effects of SGLT2 inhibition: translating insights from rats to humans in type 2 diabetes

Kidney Int. 2024 Sep;106(3):354-356. doi: 10.1016/j.kint.2024.06.018.

Abstract

The attenuation of glomerular hyperfiltration is posited to be a principal mechanism underlying the kidney protective effects of sodium-glucose cotransporter-2 (SGLT2) inhibitors in diabetic kidney disease. Notably, the impact of SGLT2 inhibitors on kidney hemodynamic function has been posited to vary between type 1 and type 2 diabetes. The study by Wada et al. documents that in an animal model of type 2 diabetes, SGLT2 inhibitors mitigate glomerular hyperfiltration predominantly through afferent arteriolar constriction, a process mediated by the adenosine/A1 receptor pathway. This observation is consistent with mechanisms identified in type 1 diabetes, arguing for similar methods in type 1 and 2 diabetes.

MeSH terms

  • Animals
  • Arterioles / drug effects
  • Arterioles / physiopathology
  • Diabetes Mellitus, Type 2* / complications
  • Diabetes Mellitus, Type 2* / drug therapy
  • Diabetes Mellitus, Type 2* / physiopathology
  • Diabetic Nephropathies* / drug therapy
  • Diabetic Nephropathies* / etiology
  • Diabetic Nephropathies* / physiopathology
  • Glomerular Filtration Rate / drug effects
  • Hemodynamics* / drug effects
  • Humans
  • Kidney / blood supply
  • Kidney / drug effects
  • Kidney / physiopathology
  • Rats
  • Sodium-Glucose Transporter 2 / metabolism
  • Sodium-Glucose Transporter 2 Inhibitors* / pharmacology
  • Sodium-Glucose Transporter 2 Inhibitors* / therapeutic use
  • Translational Research, Biomedical

Substances

  • Sodium-Glucose Transporter 2 Inhibitors
  • Sodium-Glucose Transporter 2