Treatment of renal congestion by tolvaptan
Treatment of renal congestion by tolvaptan
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托伐普坦治疗肾充血
DOI：
10.1038/s41440-019-0215-9
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发表时间：
2019
影响因子：
5.4
通讯作者：
Kinugasa Satoshi
中科院分区：
文献类型：
--
作者：
Mori Takefumi;Hirose Takuo;Kinugasa Satoshi
肾功能下降与心血管事件和死亡率增加相关，慢性肾脏疾病是心力衰竭的危险因素。相反，心力衰竭是肾功能不全的已知风险因素。因此，在心肾功能相关性的介导下，形成了一个恶性循环，这种循环在心力衰竭患者中常见，并加剧了疾病的预后[1]。值得注意的是，已知血管收缩神经激素包括肾素-血管紧张素系统、加压素和儿茶酚胺起主要作用。在心力衰竭中，动脉充盈不足刺激这些神经激素，其诱导肾缺血、缺氧和Na潴留并增强容量超负荷。在这方面，千叶等人最近的一份报告。[2]使用Dahl盐敏感大鼠和高血压心肾衰竭模型检查心肾连接的机制。他们进行了一项研究，其中在心力衰竭诱导期间测量肾脏血流动力学变化。通过肾脏超声测量局部肾血流量（RBF），并使用光纤压力传感器测量肾髓质压力。高盐饮食引起高血压心肾功能衰竭时，阻力指数和静脉阻抗指数显著增加，提示肾髓质血流量减少。
Reduced renal function is associated with increased cardiovascular events and mortality, and chronic kidney disease is a risk factor for heart failure. Conversely, heart failure is a known risk factor for renal dysfunction. Thus, a vicious cycle is formed, mediated by cardio-renal functional correlations, and this cycle is commonly observed in patients with heart failure and exacerbates the prognosis of the disease [1].Several mechanisms have been reported to be involved in the cardio-renal connection. Notably, vasoconstrictive neurohormones including the renin–angiotensin system, vasopressin and catecholamines are known to play a major role. In heart failure, arterial underfilling stimulates these neurohormones, which induce renal ischemia, hypoxia, and Na retention and enhance volume overload. In this regard, a recent report by Chiba et al.[2] examined the mechanism of the cardio-renal connection using Dahl salt-sensitive rats and a model of hypertensive cardiorenal failure. They conducted a study in which renal hemodynamic changes were measured during the induction of heart failure. Local renal blood flow (RBF) was measured by renal ultrasound, and renal medullary pressure was measured using a fiber-optic pressure sensor. The resistance index and venous impedance index were significantly increased in response to hypertensive cardio-renal failure by a high salt diet, suggesting that renal medullary blood flow was reduced.