There is a growing body of experimental and clinical evidence supporting mineralocorticoid receptor (MR) activation as a powerful mediator of renal damage in laboratory animals and humans. Multiple pathophysiological mechanisms are proposed, with the strongest evidence supporting aldosterone-induced vasculopathy, exacerbation of oxidative stress and inflammation, and increased growth factor signalling promoting fibroblast proliferation and deranged extracellular matrix homeostasis. Further involvement of the MR is supported by extensive animal model experiments where MR antagonists (such as spironolactone and eplerenone) abrogate renal injury, including ischaemia-induced damage. Additionally, clinical trials have shown MR antagonists to be beneficial in human chronic kidney disease (CKD) in terms of reducing proteinuria and cardiovascular events, though current studies have not evaluated primary end points which allow conclusions to made about whether MR antagonists reduce mortality or slow CKD progression. Although differences between human and feline CKD exist, feline CKD shares many characteristics with human disease including tubulointerstitial fibrosis. This review evaluates the evidence for the role of the MR in renal injury and summarizes the literature concerning aldosterone in feline CKD. MR antagonists may represent a promising therapeutic strategy in feline CKD.

中文翻译：

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肾损伤中的醛固酮和盐皮质激素受体：猫慢性肾病的潜在治疗靶点。

越来越多的实验和临床证据支持盐皮质激素受体 (MR) 激活作为实验室动物和人类肾脏损伤的强大介质。提出了多种病理生理机制，最有力的证据支持醛固酮诱导的血管病变、氧化应激和炎症的恶化，以及促进成纤维细胞增殖和紊乱的细胞外基质稳态的生长因子信号传导增加。MR 的进一步参与得到了广泛的动物模型实验的支持，其中 MR 拮抗剂（如螺内酯和依普利酮）消除了肾损伤，包括缺血引起的损伤。此外，临床试验表明 MR 拮抗剂在减少蛋白尿和心血管事件方面对人类慢性肾病 (CKD) 有益，尽管目前的研究尚未评估主要终点，从而可以得出关于 MR 拮抗剂是否降低死亡率或减缓 CKD 进展的结论。尽管人类和猫科动物 CKD 之间存在差异，但猫科动物 CKD 与人类疾病有许多共同特征，包括肾小管间质纤维化。本综述评估了 MR 在肾损伤中作用的证据，并总结了有关猫 CKD 中醛固酮的文献。MR 拮抗剂可能代表了猫 CKD 的一种有前途的治疗策略。本综述评估了 MR 在肾损伤中作用的证据，并总结了有关猫 CKD 中醛固酮的文献。MR 拮抗剂可能代表了猫 CKD 的一种有前途的治疗策略。本综述评估了 MR 在肾损伤中作用的证据，并总结了有关猫 CKD 中醛固酮的文献。MR 拮抗剂可能代表了猫 CKD 的一种有前途的治疗策略。