1008-P: Efficacy of Dulaglutide on Renal Functions in the Real-World Clinical Practice for Diabetes in Japan

Abstract

Aims: Efficacy of a GLP-1 receptor agonist, dulaglutide, on renal functions in type 2 diabetic patients under the real-world clinical practice in Japan was retrospectively examined. Subjects: 154 patients with type 2 diabetes treated with dulaglutide (0.75 mg once weekly) in our clinic (mean administration period 540.7 ± 332 days; mean age 58.1 years; mean duration of diabetes 10.5 years). Methods: Dulaglutide was added to the conventional antidiabetes drugs. The dose of sulfonylurea was reduced by 50-67% and all the DPP-4 inhibitors were discontinued. The annual changes in eGFR between 1 year before and 2 years after the administration of dulaglutide were retrospectively analyzed in 2 groups divided by the baseline eGFR; eGFR<90 ml/min/1.73m2 group and eGFR≧90 group. Changes in HbA1c levels and body weight were also evaluated. Results: eGFR in the eGFR<90 group (n = 90) rapidly declined (-5.4 ± 7.8/year) before the administration of dulaglutide (p <0.001). However, the decline was moderate after the administration of dulaglutide (-1.2 ± 7.1/year after 1 year, p = 0.134; -1.1 ± 5.8/year between 1 and 2 years, p = 0.179). In contrast, eGFR in the eGFR≧90 group (n = 57) was not declined before the administration of dulaglutide (+ 1.4 ± 6.6/year, p = 0.318), and significantly decreased after the administration of dulaglutide (-2.9 ± 10.0/year after 1 year, p = 0.036; -2.5 ± 6.8/year between 1 and 2 years, p = 0.048). HbA1c levels were 8.70 ± 1.76% at baseline, -1.32 ± 1.69% at 1 year (p <0.001, n = 86), -1.19 ± 1.56% at 2 years (p <0.001, n = 39). Body weight were 71.3 ± 15.2 kg at baseline, -1.86 ± 3.38 kg at 1 year (p <0.001, n = 86), -2.04±3.33 kg at 2 years (p=0.001, n=39). Conclusions: These observations suggest that dulaglutide may ameliorate renal hyperfiltration and protect renal functions. Disclosure S.T. Sato: None. 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. 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.