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Kidney Week

Abstract: FR-PO235

The Study on the Transition of Renal Function of SGLT2 Inhibitors for Type 2 Diabetes with Moderate to Severe Renal Impairment

Session Information

Category: Diabetic Kidney Disease

  • 602 Diabetic Kidney Disease: Clinical

Authors

  • Kanozawa, Koichi, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan
  • Sato, Saeko, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan
  • Kogure, Yuta, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan
  • Kurosawa, Akira, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan
  • Hatano, Minoru, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan
  • Hara, Hiroaki, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan
  • Shimizu, Taisuke, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan
  • Iwashita, Takatsugu, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan
  • Ogawa, Tomonari, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan
  • Hasegawa, Hajime, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan
Background

From the results of recent large-scale clinical trials, it has been clarified that SGLT2 inhibitors (SGLT2i) have protection of renal function independent of blood glucose. However, the renoprotective effect of SGLT2i in type 2 diabetes (T2DM) patients with advanced renal dysfunction less than eGFR 30 ml/min/1.73m2 has not been studied. The aim of study is to investigate the effect of SGLT2i on renal function in patients with moderate to severe renal insufficiency, retrospectively.

Methods

We included Japanese T2DM patients less than eGFR 45 ml/min/1.73m2, whose SGLT2i was administered for more than one year since October 2011 in Saitama madical center. We compared changes eGFR from 6 months before administration of SGLT2i to the start of administration, and from initiation of administration of SGLT2i to 6, 12 months after administration, and last month of administration (when SGLT2i is discontinued, just before discontinuation). We also examined safety.

Results

The subjects were 36 cases (12 cases were less than eGFR 30 ml/min/1.73m2), and eGFR at the start of SGLT2i administration was 33.3 ± 12.2 ml/min/1.73m2. The patients were received either ipragliflozin, canagliflozin, empagliflozin luseoglifrozin, tofoglifrozin or dapaglifrozin. The monthly change in eGFR from 6 months before to the initiation of SGLT2i administration, and from the initiation to 6, 12 months after administration, and to last chance (27 ± 13 months) were -0.7±1.3, -0.0±1.2, +0.1±0.6, and −0.0±0.4 ml/min/1.73m2/month, respectively. The decrease in eGFR was significantly suppressed after SGLT2i administration (p <0.05, respectively). During the period, renal replacement therapy (RRT) was initiated only in 3 cases. Assuming that RRT is started when eGFR 6-8 ml/min/1.73m2 remains unchanged from changes in eGFR before SGLT2i administration, it is predicted that 27 (75%) of the 36 cases could avoid RRT induction during the observation period. On the other hand, no adverse events related to SGLT2i other than RRT were observed during the period.

Conclusion


The administration of SGLT2i to T2DM with moderate to severe renal impairment can strongly and safely suppress the decline of eGFR, and can lead to enormous medical economic benefits by extending dialysis induction.