Division of Nephrology and Hypertension, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, U.S.A.
Clin Sci (Lond). 2022 Feb 11;136(3):239-256. doi: 10.1042/CS20210509.
Renovascular disease (RVD) remains a common etiology of secondary hypertension. Recent clinical trials revealed unsatisfactory therapeutic outcomes of renal revascularization, leading to extensive investigation to unravel key pathophysiological mechanisms underlying irreversible functional loss and structural damage in the chronically ischemic kidney. Research studies identified complex interactions among various players, including inflammation, fibrosis, mitochondrial injury, cellular senescence, and microvascular remodeling. This interplay resulted in a shift of our understanding of RVD from a mere hemodynamic disorder to a pro-inflammatory and pro-fibrotic pathology strongly influenced by systemic diseases like metabolic syndrome (MetS), hypertension, diabetes mellitus, and hyperlipidemia. Novel diagnostic approaches have been tested for early detection and follow-up of RVD progression, using new imaging techniques and biochemical markers of renal injury and dysfunction. Therapies targeting some of the pathological pathways governing the development of RVD have shown promising results in animal models, and a few have moved from bench to clinical research. This review summarizes evolving understanding in chronic ischemic kidney injury.
肾血管疾病（RVD）仍然是继发性高血压的常见病因。最近的临床试验显示，肾血管重建的治疗效果并不理想，这导致了广泛的研究，以揭示慢性缺血性肾脏中不可逆性功能丧失和结构损伤的关键病理生理机制。研究发现，各种因素之间存在复杂的相互作用，包括炎症、纤维化、线粒体损伤、细胞衰老和微血管重塑。这种相互作用使我们对 RVD 的理解从单纯的血流动力学障碍转变为炎症和纤维化的病理学，这受到代谢综合征（MetS）、高血压、糖尿病和高脂血症等系统性疾病的强烈影响。已经测试了新的诊断方法，以通过新的成像技术和肾功能障碍的生化标志物，对 RVD 的进展进行早期检测和随访。针对一些控制 RVD 发展的病理途径的治疗方法在动物模型中显示出了有希望的结果，并且有一些已经从基础研究转移到临床研究。这篇综述总结了慢性缺血性肾损伤方面不断发展的认识。
