Antiproteinuric Effect of Cilnidipine in Hypertensive Japanese Treated with Renin-Angiotensin-System Inhibitors - A Multicenter, Open, Randomized Trial Using 24-Hour Urine Collection

Antiproteinuric Effect of Cilnidipine in Hypertensive Japanese Treated with Renin-Angiotensin-System Inhibitors - A Multicenter, Open, Randomized Trial Using 24-Hour Urine Collection
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DOI:
10.3109/10641961003667914
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发表时间:
2010-01-01
影响因子:
12.3
通讯作者:
Matsuoka, Hiroaki
Matsuoka, Hiroaki
中科院分区:
医学4区
文献类型:
--
作者:
Miwa, Yoshikazu;Tsuchihashi, Takuya;Matsuoka, Hiroaki

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持续蛋白尿不仅是肾脏疾病,也是心血管疾病发病和死亡的重要危险因素。尽管肾素-血管紧张素系统(RAS)抑制剂已被证明可以减少蛋白尿。这些药物的单一疗法通常不足以达到最佳的降压效果,因此需要联合治疗。最近的报告表明,西尼地平是一种双重 L-/N 型钙通道阻滞剂,通过扩张传出和传入小动脉而具有肾脏保护作用。在这项研究中,设计了一项多中心、开放、随机试验,旨在比较西尼地平和氨氯地平与 RAS 抑制剂联合治疗患有明显蛋白尿的高血压患者的抗蛋白尿作用。通过收集所有患者 24 小时家庭尿液来评估蛋白尿。共有 35 名蛋白尿(>0.1 g/天)且血压未受控制(>135/85 mmHg)的患者在接受 6 个月 RAS 抑制剂治疗后被随机分配接受西尼地平(n = 18)或氨氯地平(n = 17)治疗,并随访 48 周。在基线时,与氨氯地平组相比,西尼地平组年龄较大,体重指数 (BMI) 较低。治疗 32 周后,西尼地平组的舒张压 (DBP) 略有下降,但显着降低,但收缩压 (SBP) 和平均血压没有差异。基线时尿蛋白没有差异(西尼地平组 0.48 g/天,氨氯地平组 0.52 g/天);然而,治疗48周后,与氨氯地平组(0.50克/天)相比,西尼地平组(0.22克/天)显着下降。我们的研究结果表明,即使在接受 RAS 抑制剂治疗的高血压患者中,西尼地平在预防蛋白尿进展方面也优于氨氯地平。
Sustained proteinuria is an important risk factor for not only renal but also cardiovascular morbidity and mortality. Although inhibitors of the renin-angiotensin system (RAS) have been shown to reduce proteinuria. Monotherapy with those drugs is often insufficient for optimal blood pressure (BP)-lowering and therefore, combined therapy is needed. Recent reports suggested that cilnidipine, a dual L-/N-type calcium channel blocker, has renoprotective effect by dilating both efferent and afferent arterioles. In this study, a multicenter, open, randomized trial was designed to compare the antiproteinuric effect between cilnidipine and amlodipine when coupled with RAS inhibitors in hypertensive patients with significant proteinuria. Proteinuria was evaluated by 24-h home urine collection for all patients. A total of 35 proteinuric (>0.1 g/day) patients with uncontrolled BP (>135/85 mmHg) were randomized to receive either cilnidipine (n = 18) or amlodipine (n = 17) after a 6-month treatment with RAS inhibitors and were followed for 48 weeks. At baseline, the cilnidipine group was older and had lower body mass index (BMI) compared to the amlodipine group. After 32 weeks of treatment, diastolic blood pressure (DBP) was slightly, but significantly reduced, in the cilnidipine group, although systolic blood pressure (SBP) and mean BP did not differ. The urinary protein did not differ at baseline (cilnidipine group 0.48 g/day, amlodipine group 0.52 g/day); however, it significantly decreased in the cilnidipine group (0.22 g/day) compared to the amlodipine group (0.50 g/day) after 48 weeks of treatment. Our findings suggest that cilnidipine is superior to amlodipine in preventing the progression of proteinuria in hypertensive patients even undergoing treatment with RAS inhibitors.