Division of Nephrology, University of Southern California, LAC+USC Medical Center, 2020 Zonal Avenue IRD 806, Los Angeles, CA 90033, USA.
Curr Hypertens Rep. 2010 Aug;12(4):303-6. doi: 10.1007/s11906-010-0116-4.
There has been much recent interest in the role of aldosterone as an independent contributor to the progression of chronic kidney disease. Despite treatment with agents such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, many studies have shown that there is incomplete blockade of the renin-angiotensin cascade evidenced by persistent or rising plasma aldosterone levels despite therapeutic renin-angiotensin blockade. This phenomenon is commonly referred to as "aldosterone escape" and is thought to be one of the main contributors to chronic kidney disease progression despite conventional therapeutics. Animal models of the effects of exposure to exogenous aldosterone demonstrate the development of inflammation and fibrosis in both the myocardium and renal parenchyma. In limited human studies, aldosterone receptor antagonism is associated with decreased proteinuria and improved glomerular filtration rate. Although data support the addition of an aldosterone antagonist to conventional therapy when treating patients with chronic kidney disease, more studies are needed to determine the precise clinical indications and the appropriate safety monitoring.
最近，人们对醛固酮在慢性肾脏病进展中的作用产生了浓厚的兴趣。尽管使用了血管紧张素转换酶抑制剂和血管紧张素受体阻滞剂等药物进行治疗，但许多研究表明，尽管进行了肾素-血管紧张素阻断治疗，但肾素-血管紧张素级联反应并未完全阻断，表现为血浆醛固酮水平持续或升高。这种现象通常被称为“醛固酮逃逸”，被认为是尽管采用常规疗法但导致慢性肾脏病进展的主要因素之一。暴露于外源性醛固酮的动物模型研究表明，心肌和肾实质均会发生炎症和纤维化。在有限的人类研究中，醛固酮受体拮抗剂与蛋白尿减少和肾小球滤过率改善相关。尽管数据支持在治疗慢性肾脏病患者时将醛固酮拮抗剂添加到常规治疗中，但仍需要更多的研究来确定确切的临床适应证和适当的安全监测。
