Kidney Week

Abstract: SA-PO0210

Investigation of the Inhibitory Effects of Empagliflozin on Tubular Oxidative Stress in a Nondiabetic Rat Model of Early-Stage CKD

Session Information

• CKD: Mechanisms of Injury and Fibrosis - 3
  October 24, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: CKD (Non-Dialysis)

• 2203 CKD (Non-Dialysis): Mechanisms

Authors

• Moriya, Reika Flora, Fukushima Kenritsu Ika Daigaku, Fukushima, Fukushima Prefecture, Japan

Reika Flora Moriya, MD

• Horita, Shoichiro, Fukushima Kenritsu Ika Daigaku, Fukushima, Fukushima Prefecture, Japan

Shoichiro Horita, PhD

• Higashi, Atsuko Y., Fukushima Kenritsu Ika Daigaku, Fukushima, Fukushima Prefecture, Japan

Atsuko Y. Higashi, MD, PhD

• Tanaka, Kenichi, Fukushima Kenritsu Ika Daigaku, Fukushima, Fukushima Prefecture, Japan

Kenichi Tanaka, MD, PhD

• Shimabukuro, Michio, Fukushima Kenritsu Ika Daigaku, Fukushima, Fukushima Prefecture, Japan

Michio Shimabukuro, MD, PhD

• Kazama, Junichiro James, Fukushima Kenritsu Ika Daigaku, Fukushima, Fukushima Prefecture, Japan

Junichiro James Kazama, MD, PhD

Background

While substantial evidence supports the role of empagliflozin, a sodium–glucose cotransporter 2(SGLT2) inhibitor, in preventing the progression of chronic kidney disease (CKD), the underlying mechanisms remain incompletely understood. Although previous studies have reported that empagliflozin reduces tubular injury and oxidative stress in diabetic rat models, its effects on non-diabetic, mild renal insufficiency models such as the 1/2 nephrectomy model, have not been fully explored.

Methods

In this study, we investigated the effects of empagliflozin on creatinine clearance (CCr) and renal tissue in non-diabetic CKD rats.

Results

Long-term administration of empagliflozin showed no significant differences in body weight, urine volume, or CCr compared to the control group. However, spatial analysis via imaging mass cytometry (IMC) revealed a significant reduction in oxidative stress markers specifically within the renal tubules of the empagliflozin group, whereas no such change was observed in the glomeruli. Furthermore, plasma NT-proBNP levels showed no significant difference, suggesting that the observed effects were not primarily driven by systemic cardio-renal interactions.

Conclusion

These findings suggest that empagliflozin attenuates tubular oxidative stress in non-diabetic CKD models, even at a stage prior to detectable changes in CCr. Since the efficacy of empagliflozin may vary depending on the model, age, and severity of renal impairment, further investigation is warranted.