Low-renin hypertension (LRH) is a frequent condition in patients with arterial hypertension, accounting for 30% of patients. Monogenic forms can cause LRH in a minority of cases. However, in the large majority of patients, LRH is caused by the combined effects of congenital and acquired factors, comprising dietary habits. Several genetic variants have been proposed as co-factors in the pathogenesis of LRH with normal-low serum aldosterone. Emerging evidences support the hypothesis that a large proportion of LRH with normal-high serum aldosterone is associated with subclinical primary aldosteronism (PA). The recent identification of aldosterone-producing cell clusters (APCCs) as the possible cause of subclinical PA, further supported the concept of a continuous spectrum of autonomous aldosterone secretion, from subclinical forms towards overt PA. In this review we describe the main aspects of LRH, focusing on molecular basis, clinical risk profile and patients’ management.

低肾素高血压（LRH）是动脉高血压患者的常见病，占患者的30％。单基因形式可在少数情况下引起LRH。但是，在大多数患者中，LRH是由包括饮食习惯在内的先天性因素和后天因素共同作用引起的。已经提出了几种遗传变异作为正常低血清醛固酮在LRH发病中的辅助因素。越来越多的证据支持以下假设：LRH的血清醛固酮水平偏高通常与亚临床原发性醛固酮增多症（PA）有关。醛固酮生产细胞簇（APCC）的最新鉴定是亚临床PA的可能病因，进一步支持了从亚临床形式到明显PA的连续性醛固酮分泌自动谱的概念。