Yoshimoto Takuo, Furuki Takayuki, Kobori Hiroyuki, Miyakawa Masaaki, Imachi Hitomi, Murao Koji, Nishiyama Akira
Department of Endocrinology and Metabolism, Faculty of Medicine, Kagawa University, Miki - cho, Kagawa, Japan.
Department of Medicine, Hadanoeki - Minamiguchi Clinic, Hadano, Kanagawa, Japan.
J Investig Med. 2017 Oct;65(7):1057-1061. doi: 10.1136/jim-2017-000445. Epub 2017 Jun 8.
We conducted a descriptive case study to examine the effects of sodium-glucose cotransporter 2 (SGLT2) inhibitors on urinary angiotensinogen excretion, which represents the function of the intrarenal renin-angiotensin system, in patients with type 2 diabetes. An SGLT2 inhibitor (canagliflozin 100 mg/day, ipragliflozin 25 mg/day, dapagliflozin 5 mg/day, luseogliflozin 2.5 mg/day or tofogliflozin 20 mg/day) was administered for 1 month (n=9). ELISA kits were used to measure both urinary intact and total angiotensinogen levels. Treatment with SGLT2 inhibitors significantly decreased hemoglobin A1c, body weight, systolic blood pressure and diastolic blood pressure (8.5±1.3 to 7.5%±1.0%, 82.5±20.2 to 80.6±20.9 kg, 143±8 to 128±14 mm Hg, 78±10 to 67±9 mm Hg, p<0.05, respectively), while urinary albumin/creatinine ratio was not significantly changed (58.6±58.9 to 29.2±60.7 mg/g, p=0.16). Both total urinary angiotensinogen/creatinine ratio and intact urinary angiotensinogen/creatinine ratio tended to decrease after administration of SGLT2 inhibitors. However, these changes were not significant (p=0.19 and p=0.08, respectively). These data suggest that treatment with SGLT2 inhibitors does not activate the intrarenal renin-angiotensin system in patients with type 2 diabetes.
我们开展了一项描述性病例研究，以探讨钠-葡萄糖协同转运蛋白2（SGLT2）抑制剂对2型糖尿病患者尿血管紧张素原排泄的影响，尿血管紧张素原排泄代表肾内肾素-血管紧张素系统的功能。给予一种SGLT2抑制剂（卡格列净100毫克/天、依帕列净25毫克/天、达格列净5毫克/天、鲁格列净2.5毫克/天或托格列净20毫克/天），持续给药1个月（n = 9）。使用酶联免疫吸附测定（ELISA）试剂盒测量尿中完整血管紧张素原水平和总血管紧张素原水平。SGLT2抑制剂治疗可显著降低糖化血红蛋白、体重、收缩压和舒张压（分别从8.5±1.3%降至7.5%±1.0%、从82.5±20.2千克降至80.6±20.9千克、从143±8毫米汞柱降至128±14毫米汞柱、从78±10毫米汞柱降至67±9毫米汞柱，p<0.05），而尿白蛋白/肌酐比值无显著变化（从58.6±58.9毫克/克降至29.2±60.7毫克/克，p = 0.16）。给予SGLT2抑制剂后，尿总血管紧张素原/肌酐比值和尿完整血管紧张素原/肌酐比值均有下降趋势。然而，这些变化并不显著（分别为p = 0.19和p = 0.08）。这些数据表明，SGLT2抑制剂治疗不会激活2型糖尿病患者的肾内肾素-血管紧张素系统。
