In patients with acute kidney injury progressively converting into chronic kidney disease (CKD), proteinuria and high blood pressure predict progression to end-stage renal disease (ESRD). Although, Renin-angiotensin-aldosterone system (RAAS) regulates blood pressure and kidney disease through both direct and indirect mechanisms. RAAS blockers that act at the level of angiotensin or lower in the cascade can cause compensatory increases in the plasma renin and angiotensin II level. Here, in this review article, we are exploring the evidence-based on RAAS blockade action releases of aldosterone and hypothesizing the molecular mechanism for converting the acute kidney injury into chronic kidney disease to end-stage renal disease.

中文翻译：

---

RAAS阻滞剂的单药治疗和醛固酮的动员：肾脏疾病的机制研究。

在患有急性肾损伤的患者中，逐渐将其转化为慢性肾病（CKD），蛋白尿和高血压可预测其发展为终末期肾病（ESRD）。虽然，肾素-血管紧张素-醛固酮系统（RAAS）通过直接和间接机制调节血压和肾脏疾病。作用于级联反应中血管紧张素水平或更低水平的RAAS阻滞剂可导致血浆肾素和血管紧张素II水平的代偿性增加。在本文中，我们正在研究基于醛固酮的RAAS阻断作用释放的证据，并假设了将急性肾损伤转化为慢性肾病至终末期肾病的分子机制。