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The spectrum of low-renin hypertension.

F. Buffolo,S. Monticone,6 Authors,P. Mulatero

2020 · DOI: 10.1016/j.beem.2020.101399
Best practice & research. Clinical endocrinology & metabolism · 20 Citations

TLDR

The hypothesis that a large proportion of LRH with normal-high serum aldosterone is associated with subclinical primary aldosteronism (PA) is supported, and the concept of a continuous spectrum of autonomous ald testosterone secretion, from subclinical forms towards overt PA is supported.

Abstract

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.