获得性继发性醛固酮缺乏症（选择性低肾素性低醛固酮血症）于1957年由Hudson首先报告。患者醛固酮减少的原因为肾素缺乏，临床特点为高钾血症、血浆肾素和醛固酮降低和高氯性酸中毒（Ⅳ型肾小管性酸中毒）。

AT-2是刺激醛固酮分泌的最关键因素。许多肾脏疾病均可干扰或破坏肾小球球旁装置，导致肾素缺乏和继发性醛固酮缺乏，即低肾素血症性低醛固酮症（hyporeninemic hypoaldosteronism），其病因包括：①慢性肾脏疾病：如糖尿病肾病、慢性肾盂肾炎、间质性肾炎、肾小球硬化、肾囊肿和肾石病。②其他疾病和因素所致的肾损伤：如狼疮性肾炎、痛风、多发性骨髓瘤、肾脏淀粉样变性或甲旁亢。③药物：如肾素分泌抑制剂、前列腺素合酶抑制剂、环孢素（cyclosporin A）、丝裂霉素C（mitomycin C）、ACTH、替可克肽（cosyntropin）、非甾体类抗炎药、两性霉素和止痛药等。④垂体选择性ACTH缺乏症。⑤其他：如先天性自主神经病变、肝硬化、镰状细胞贫血、POEMS综合征、AIDS、铅中毒、过量使用碳酸氢钠、血色病等。但在临床上，以糖尿病肾病最常见。肾素和醛固酮分泌减少涉及多个方面，主要有：①肾功能损害，肾小球滤过减少，血容量增加，血压增高，肾素分泌减少。②肾间质性疾病损害肾小球球旁器，分泌肾素的颗粒细胞数目减少，肾素释放减少，继发醛固酮分泌不足。尸检发现患有本病的糖尿病肾病患者，肾小球球旁器有透明变性。③自主神经病变（尤其是糖尿病自主神经病变）使肾素释放减少。④肾素原转化为肾素存在缺陷。GH缺乏也可导致低肾素低醛固酮症，原因不明。

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