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Low-renin hypertension (LRH) affects approximately 30 percent of patients with arterial hypertension and represents a spectrum of heterogeneous disorders characterized by low renin levels, increased sodium reabsorption, and expanded circulating volume. LRH includes monogenic and acquired secondary forms; however, the majority of the patients-particularly older individuals and those of African descent-present essential hypertension. Primary aldosteronism is the most frequent secondary cause, marked by excessive and autonomous aldosterone secretion. Other monogenic forms, such as Liddle syndrome, apparent mineralocorticoid excess and familial hyperkalaemic hypertension, are distinguished by specific biochemical and genetic profiles. Acquired causes of LRH include high dietary sodium intake, renal diseases, drugs inhibiting the renin-angiotensin-aldosterone system, and exogenous or endogenous factors like high consumption of mineralocorticoid-like substances (i.e. licorice) or cortisol excess. Careful clinical evaluation, including family history, and measurement of renin, aldosterone, and potassium levels are essential for accurate diagnosis and tailored treatment. Mineralocorticoid receptor activation and/or increased sodium reabsorption are a common mechanism in the pathogenesis of LRH, with a continuum between essential and secondary forms. Recognizing these subtypes has significant therapeutic implications, as targeted treatments can improve long-term outcomes and reduce cardiovascular events. This chapter describes the differential diagnosis and underlying mechanisms of the most common conditions presenting with a LRH phenotype, with a focus on diagnostic and therapeutic approaches.