Protection of the kidney with sodium-glucose cotransporter 2 inhibitors: potential mechanisms raised by the

Satoru Kuriyama1

  • 1Miho Clinic, Jikei University School of Medicine, Shin-Osaki Kangyo Bldg. 2F, 1-6-4, Osaki, Shinagawa-ku, 141-0032, Tokyo, Japan. kuriyamas218@yahoo.co.jp.

Insights

Sodium-glucose cotransporter 2 (SGLT2) inhibitors offer renal protection in diabetics. This review explores mechanisms beyond hemodynamics, including uric acid, lipids, and oxidative stress.

Area of Science:

  • Nephrology
  • Cardiology
  • Endocrinology

Background:

  • Sodium-glucose cotransporter 2 (SGLT2) inhibitors have demonstrated significant cardio-renal protective effects.
  • Key trials like CANVAS Program and EMPA-REG OUTCOME have spurred research into their mechanisms.
  • Existing literature offers varied explanations for these protective effects.

Purpose of the Study:

  • To provide a current overview of the renal protective effects of SGLT2 inhibitors in diabetic patients.
  • To focus on the hemodynamic aspects and under-explored factors contributing to renal protection.
  • To address unanswered questions regarding uric acid, lipids, erythropoiesis, oxidative stress, and the Na-H exchanger.

Main Methods:

  • Literature review and synthesis of existing research.
  • Focus on hemodynamic mechanisms of SGLT2 inhibition.
  • Exploration of less-discussed factors influencing renal protection.

Main Results:

  • SGLT2 inhibitors exhibit established hemodynamic benefits relevant to renal protection.
  • Several other factors, including uric acid, lipids, erythropoiesis, oxidative stress, and Na-H exchange, are implicated but require further investigation.
  • Discrepancies exist in the literature regarding the precise mechanisms.

Conclusions:

  • SGLT2 inhibitors provide renal protection in diabetics through multiple pathways.
  • Further research is needed to fully elucidate the roles of uric acid, lipids, oxidative stress, and other factors.
  • A comprehensive understanding of these mechanisms is crucial for optimizing SGLT2 inhibitor therapy.

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