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肾脏调节全身的体液量,这种调节是持续性的,并且与血压的调节有很大关系。一方面,肾脏可视为高血压损害的靶器官,肾脏一旦受损,高血压的发生率增加。高血压引起的肾损害病理学表现为肾硬化症,功能表现为肾血流量减少,出现蛋白尿。但是,高血压引起肾小球硬化、肾脏血流减少以及蛋白尿的机制尚不明确。此外,大规模的临床试验表明血管紧张素转换酶(ACE)抑制剂和血管紧张素Ⅱ(AⅡ)受体拮抗剂不仅可降低血压,也可减少尿蛋白、抑制肾功能减退,具有肾脏保护作用。本文简介高血压性肾损害的病理生理和应用肾素-血管紧张素(R-A)系统抑制剂的治疗。
The kidneys regulate the amount of body fluid throughout the body, and this regulation is persistent and has a great relationship with the regulation of blood pressure. On the one hand, the kidneys can be regarded as target organs of hypertension damage, once the kidney is damaged, the incidence of hypertension is increased. Hypertension caused by renal damage pathological manifestations of renal sclerosis, the performance of renal blood flow decreased proteinuria. However, the mechanisms by which high blood pressure causes glomerulosclerosis, renal blood flow, and proteinuria are unclear. In addition, large-scale clinical trials have shown that angiotensin converting enzyme (ACE) inhibitors and angiotensin II (AII) receptor antagonists not only lower blood pressure, but also reduce urinary protein, inhibit renal dysfunction and have renal protective effect . This article describes the pathophysiology of hypertensive renal impairment and the use of renin-angiotensin (R-A) system inhibitors.