Nomoto Hidetsugu, Satoh Yasuhiro, Kamiyama Mayu, Yabe Kento, Masumura Mayumi, Sakakibara Atsushi, Yamashita Shu, Suzuki Masahito, Sugiyama Tomoyo, Oumi Tetsuo, Ohno Masakazu, Takahashi Yoshihide, Isobe Mitsuaki
Department of Cardiovascular Medicine, National Hospital Organization, Disaster Medical Center.
Department of Cardiovascular Medicine, Tokyo Medical and Dental University.
Int Heart J. 2017 Aug 3;58(4):593-600. doi: 10.1536/ihj.16-438. Epub 2017 Jul 13.
Tolvaptan, a vasopressin type 2 receptor antagonist, does not affect kidney circulation or cause worsening of renal function (WRF) in patients with acute decompensated heart failure (ADHF). Bioelectrical impedance analysis (BIA) can be used to evaluate intravascular volume by calculating the ratio of extracellular water (ECW) to intracellular water (ICW). There have been no reports examining the mechanisms of tolvaptan-induced diuresis using BIA. We investigated whether tolvaptan decreases excess volume while maintaining intravascular volume in ADHF patients.Study patients included 29 ADHF patients (age 48-95, men 69%) diagnosed between April 2013 and May 2016 and who underwent BIA before and after treatment. Fifteen patients were treated with tolvaptan in addition to conventional diuresis therapy (tolvaptan group), and 14 patients were treated with conventional diuresis therapy only (control group). In the control group, the numerical value of serum creatinine (Cre) significantly increased from 0.89 ± 0.22 mg/ dL to 1.07 ± 0.29 mg/dL (P = 0.004), and the ECW/ICW significantly decreased from 0.696 ± 0.036 to 0.673 ± 0.032 (P = 0.004). These values were not significantly different from those obtained for the tolvaptan group. Furthermore, regression analysis showed a negative correlation between ΔCre and ΔECW/ICW, which are the differences between values before and after treatment (ΔCre = -0.002-5.668 × ΔECW/ICW, r = 0.306, P = 0.002).Our findings suggest that WRF is caused by a reduction in intravascular volume and that tolvaptan treatment can decrease the excess volume while maintaining intravascular volume.
托伐普坦是一种血管加压素2型受体拮抗剂，对急性失代偿性心力衰竭（ADHF）患者的肾循环无影响，也不会导致肾功能恶化（WRF）。生物电阻抗分析（BIA）可通过计算细胞外液（ECW）与细胞内液（ICW）的比值来评估血管内容量。目前尚无关于使用BIA研究托伐普坦诱导利尿机制的报道。我们研究了托伐普坦在维持ADHF患者血管内容量的同时是否能减少过多的容量。研究患者包括29例在2013年4月至2016年5月期间确诊的ADHF患者（年龄48 - 95岁，男性占69%），这些患者在治疗前后均接受了BIA检查。15例患者在常规利尿治疗基础上加用托伐普坦（托伐普坦组），14例患者仅接受常规利尿治疗（对照组）。对照组中，血清肌酐（Cre）数值从0.89±0.22mg/dL显著升高至1.07±0.29mg/dL（P = 0.004），ECW/ICW从0.696±0.036显著降至0.673±0.032（P = 0.004）。这些数值与托伐普坦组获得的数值无显著差异。此外，回归分析显示治疗前后差值（ΔCre）与ΔECW/ICW之间呈负相关（ΔCre = -0.002 - 5.668×ΔECW/ICW，r = 0.306，P = 0.002）。我们的研究结果表明，肾功能恶化是由血管内容量减少引起的，托伐普坦治疗可在维持血管内容量的同时减少过多的容量。
