SGLT2 抑制剂可纠正成人肾移植受者的体液超负荷--一项前瞻性观察研究

Anja Schork, Marie-Luise Eberbach, Ferruh Artunc, Bernhard N. Bohnert, Felix Eisinger, David J. Heister, Dorothea Vosseler, Silvio Nadalin, A. Birkenfeld, Nils Heyne, Martina Guthoff
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引用次数: 0

摘要

在这项纵向观察研究中,我们测量了 n = 22 名肾移植受者(KTRs)在开始使用 SGLT2I 时的尿糖浓度、身体成分和容量状态(生物阻抗光谱)以及血浆肾素和醛固酮浓度,这些数据分别来自基线(BL)、1 周后、1、3 和 6 个月后。估计肾小球滤过率(eGFR)在 1 周后下降了 -2 mL/min/1.73 m2(IQR -10-0),此后保持稳定。1 周后尿糖浓度为 10 (3-24) g/g 肌酐,并与 eGFR 相关(r2 = 0.273; p = 0.057)。SGLT2I 不影响 HbA1c、空腹血糖、体重、脂肪或瘦体重。SGLT2I 能减轻液体超负荷,这与基线过量脱水有关(OH,r2 = 0.54,p = 0.0003),但不会出现脱水。血浆醛固酮在第 7 天有所增加,而血浆肾素没有显著变化。总之,SGLT2I 可纠正基线过量脱水患者的体液超负荷,而无水 KTR 患者的体液状态保持稳定,体内水分未降至参考范围以下,从而提高了肾移植患者接受 SGLT2I 治疗的安全性。葡萄糖尿以及 SGLT2I 对血糖控制和体重的影响在依赖于 eGFR 的 KTR 中有所减轻。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
SGLT2 Inhibitors Correct Fluid Overload in Adult Kidney Transplant Recipients—A Prospective Observational Study
In this longitudinal observational study, we measured urinary glucose concentration, body composition and volume status (bioimpedance spectroscopy) and plasma renin and aldosterone concentrations in n = 22 kidney transplant recipients (KTRs) initiating on SGLT2I at baseline (BL), and after 1 week and 1, 3, and 6 months. Estimated glomerular filtration rate (eGFR) decreased by −2 mL/min/1.73 m2 (IQR −10–0) after 1 week and remained stable thereafter. Urinary glucose concentration was 10 (3–24) g/g creatinine after 1 week and correlated with eGFR (r2 = 0.273; p = 0.057). SGLT2I did not affect HbA1c, fasting blood glucose, body weight, fat or lean mass. SGLT2I decreased fluid overload dependent on baseline overhydration (OH, r2 = 0.54, p = 0.0003) without occurrence of dehydration. Plasma aldosterone increased at day 7, while plasma renin did not change significantly. In conclusion, SGLT2I corrected fluid overload in patients with elevated overhydration at baseline, while in euvolemic KTRs fluid status remained stable without reduction of body water below the reference range, thus promoting the safety of SGLT2I therapy in patients following kidney transplantation. Glucosuria, together with effects of SGLT2I on blood glucose control and body weight, is attenuated in KTRs dependent on eGFR.
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