Effects of SGLT2 inhibitors (SGLT2i) on renal functions were examined in patients with type 2 diabetes followed by our clinic. Subjects were 395 outpatients treated with SGLT2i (ipragliflozin 135; empagliflozin 101; canagliflozin 83; dapagliflozin 76; age 51.6 ± 11.3 years; duration of diabetes 7.21 ± 6.8 years; BMI 28.6 ± 4.5). Changes in eGFR at 1 year before and 2 years after the administration of SGLT2i versus at baseline were retrospectively analyzed in 2 groups divided by the baseline eGFR; eGFR<90 ml/min/1.73m2 group and eGFR≧90 group. The changes in urinary albumin excretion rate (UAER) and HbA1c levels were also examined. The average values of each four measures in a year were used as the levels for each period. In the eGFR<90 group (n = 179), the annual change in eGFR (ΔGFR) was -2.1 ± 5.5/year before administration of SGLT2i (p <0.001), -1.4 ± 7.5/year after 1 year (p = 0.020) and +0.2 ± 5.9/year between 1 and 2 years (p = 0.704). In the eGFR≧90 group (n = 164), ΔGFR was -1.2 ± 8.0/year before administration of SGLT2i (p = 0.180), -3.2 ± 11.6/year after 1 year (p = 0.001) and -1.2 ± 8.2/year between 1 and 2 years (p = 0.133). In the group with ΔGFR?-5/year before administration of SGLT2i (n = 56), ΔGFR was -9.1 ± 3.5/year before administration (p <0.001), -0.9 ± 8.9/year after 1 year (p = 0.473) and -2.4 ± 10.6/year between 1 and 2 years (p = 0.176). In the group with ΔGFR >-5/year before administration (n = 137), ΔGFR was +1.9 ± 5.3/year before administration (p <0.001), -4.1 ± 9.5/year after 1 year (p <0.001) and +0.6 ± 6.0/year between 1 and 2 years (p = 0.306). UAER changes in total subjects were +41.1 ± 267.5 mg/g creatinine/year before administration of SGLT2i (p = 0.039), -8.8 ± 220.1/year after 1 year (p = 0.474) and +8.0 ± 88.0/year between 1 and 2 years (p = 0.144).

HbA1c levels were 7.27 ± 1.19% and 7.67 ± 1.31 at 1 year before and baseline, respectively, and decreased at 2 years (-0.49 ± 1.16%, p <0.001, n = 145). These observations suggest that SGLT2i may have protective effects on renal functions in the real-world clinical practice.

Disclosure

T. Tosaki: Research Support; Self; Daiichi Sankyo Company, Limited, Sanofi K.K. Speaker's Bureau; Self; Astellas Pharma Inc., Eli Lilly and Company, Merck Sharp & Dohme Corp., Sumitomo Dainippon Pharma Co., Ltd., Takeda Pharmaceutical Company Limited. S.T. Sato: None. M. Kondo: None. Y. Yamada: None. A. Inagaki: None. S. Tsunekawa: None. T. Himeno: None. Y. Kato: Speaker's Bureau; Self; Merck & Co., Inc. J. Nakamura: Research Support; Self; Astellas Pharma Inc., Boehringer Ingelheim Pharmaceuticals, Inc., Daiichi Sankyo Company, Limited, Eli Lilly and Company, Japan Tobacco Inc., Kissei Pharmaceutical Co., Ltd., Merck Sharp & Dohme Corp., Novartis Pharmaceuticals Corporation, Novo Nordisk Inc., Ono Pharmaceutical Co., Ltd., Sanofi K.K., Sumitomo Dainippon Pharma Co., Ltd., Taisho Pharmaceutical Co., Ltd., Takeda Pharmaceutical Company Limited. Speaker's Bureau; Self; Astellas Pharma Inc., AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Daiichi Sankyo Company, Limited, Eli Lilly and Company, Kowa Pharmaceu. Co. Ltd., Merck Sharp & Dohme Corp., Mitsubishi Tanabe Pharma Corporation, Novartis Pharmaceuticals Corporation, Novo Nordisk Inc., Ono Pharmaceutical Co., Ltd., Sanofi K.K., Takeda Pharmaceutical Company Limited, Terumo Medical Corporation. H. Kamiya: Speaker's Bureau; Self; Astellas Pharma Inc., Eli Lilly Japan K.K., MSD K.K., Novartis Pharma K.K., Novo Nordisk Oharma Ltd., Ono Pharmaceutical Co., Ltd., Sanofi K.K.

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