Department of Medicine, Division of Nephrology, University of Ottawa, Ottawa, ON K1H 8L6, Canada.
Clinical Epidemiology Program, Ottawa Hospital Research Institute, Ottawa, ON K1H 8L6, Canada.
Endocr Rev. 2024 Jan 4;45(1):69-94. doi: 10.1210/endrev/bnad024.
Primary aldosteronism (PA) is an endocrinopathy characterized by dysregulated aldosterone production that occurs despite suppression of renin and angiotensin II, and that is non-suppressible by volume and sodium loading. The effectiveness of surgical adrenalectomy for patients with lateralizing PA is characterized by the attenuation of excess aldosterone production leading to blood pressure reduction, correction of hypokalemia, and increases in renin-biomarkers that collectively indicate a reversal of PA pathophysiology and restoration of normal physiology. Even though the vast majority of patients with PA will ultimately be treated medically rather than surgically, there is a lack of guidance on how to optimize medical therapy and on key metrics of success. Herein, we review the evidence justifying approaches to medical management of PA and biomarkers that reflect endocrine principles of restoring normal physiology. We review the current arsenal of medical therapies, including dietary sodium restriction, steroidal and nonsteroidal mineralocorticoid receptor antagonists, epithelial sodium channel inhibitors, and aldosterone synthase inhibitors. It is crucial that clinicians recognize that multimodal medical treatment for PA can be highly effective at reducing the risk for adverse cardiovascular and kidney outcomes when titrated with intention. The key biomarkers reflective of optimized medical therapy are unsurprisingly similar to the physiologic expectations following surgical adrenalectomy: control of blood pressure with the fewest number of antihypertensive agents, normalization of serum potassium without supplementation, and a rise in renin. Pragmatic approaches to achieve these objectives while mitigating adverse effects are reviewed.
原醛症（PA）是一种内分泌疾病，其特征是尽管肾素和血管紧张素 II 受到抑制，但醛固酮的产生仍然失调，且不能通过容量和钠负荷来抑制。对于侧化 PA 患者，手术肾上腺切除术的有效性表现为过度醛固酮产生的减弱，导致血压降低、低钾血症纠正，以及肾素生物标志物的增加，这些共同表明 PA 病理生理学的逆转和正常生理学的恢复。尽管绝大多数 PA 患者最终将接受药物治疗而不是手术治疗，但缺乏关于如何优化药物治疗以及成功的关键指标的指导。在此，我们回顾了支持 PA 药物治疗方法和反映恢复正常生理学的内分泌原则的生物标志物的证据。我们回顾了当前的药物治疗武器库，包括饮食钠限制、甾体和非甾体盐皮质激素受体拮抗剂、上皮钠通道抑制剂和醛固酮合酶抑制剂。至关重要的是，临床医生认识到，当有意滴定时，PA 的多模式药物治疗可以非常有效地降低不良心血管和肾脏结局的风险。反映优化药物治疗的关键生物标志物与手术后的生理预期惊人地相似：用最少数量的降压药物控制血压、无需补充即可使血清钾正常化，以及肾素升高。同时减轻不良反应的实用方法也进行了讨论。
