Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN (A.E., L.O.L.).
Department of Medical Pharmacology and Physiology, University of Missouri-Columbia (A.R.C.).
Hypertension. 2024 Feb;81(2):206-217. doi: 10.1161/HYPERTENSIONAHA.123.21362. Epub 2023 Oct 23.
Almost a hundred years have passed since obstruction of the renal artery has been recognized to raise blood pressure. By now chronic renovascular disease (RVD) due to renal artery stenosis is recognized as a major source of renovascular hypertension and renal disease. In some patients, RVD unaccompanied by noteworthy renal dysfunction or blood pressure elevation may be incidentally identified during peripheral angiography. Nevertheless, in others, RVD might present as a progressive disease associated with diffuse atherosclerosis, leading to loss of renal function, renovascular hypertension, hemodynamic compromise, and a magnified risk for cardiovascular morbidity and mortality. Atherosclerotic RVD leads to renal atrophy, inflammation, and hypoxia but represents a potentially treatable cause of chronic renal failure because until severe fibrosis sets in the ischemic kidney, it retains a robust potential for vascular and tubular regeneration. This remarkable recovery capacity of the kidney begs for early diagnosis and treatment. However, accumulating evidence from both animal studies and randomized clinical trials has convincingly established the inadequate efficacy of renal artery revascularization to fully restore renal function or blood pressure control and has illuminated the potential of therapies targeted to the ischemic renal parenchyma to instigate renal regeneration. Some of the injurious mechanisms identified as potential therapeutic targets included oxidative stress, microvascular disease, inflammation, mitochondrial injury, and cellular senescence. This review recapitulates the intrinsic mechanisms that orchestrate renal damage and recovery in RVD and can be harnessed to introduce remedial opportunities.
自肾动脉阻塞被发现会导致血压升高以来，已经过去了近一百年。如今，由于肾动脉狭窄引起的慢性肾血管疾病（RVD）已被认为是肾血管性高血压和肾脏疾病的主要来源。在一些患者中，在进行外周血管造影时可能会偶然发现不伴有明显肾功能障碍或血压升高的 RVD。然而，在其他患者中，RVD 可能表现为一种进行性疾病，与弥漫性动脉粥样硬化有关，导致肾功能丧失、肾血管性高血压、血液动力学受损，以及心血管发病率和死亡率的风险增加。动脉粥样硬化性 RVD 导致肾脏萎缩、炎症和缺氧，但它是慢性肾衰竭的潜在可治疗原因，因为在严重纤维化发生之前，缺血性肾脏仍具有强大的血管和管状再生潜力。肾脏的这种惊人恢复能力需要早期诊断和治疗。然而，来自动物研究和随机临床试验的累积证据令人信服地证实了肾动脉血运重建不足以完全恢复肾功能或血压控制，并阐明了针对缺血性肾实质的治疗方法引发肾脏再生的潜力。一些被确定为潜在治疗靶点的损伤机制包括氧化应激、微血管疾病、炎症、线粒体损伤和细胞衰老。这篇综述回顾了 RVD 中协调肾脏损伤和恢复的内在机制，并可以利用这些机制来引入补救机会。
