Taweesak Wannachalee1,2, Adina F Turcu3. 1. Division of Metabolism, Endocrinology, and Diabetes, University of Michigan, 1150 W Medical Center Drive, MSRB II, 5570B, Ann Arbor, MI, 48109, USA. 2. Division of Endocrinology and Metabolism, Siriraj Hospital, Mahidol University, Bangkok, Thailand. 3. Division of Metabolism, Endocrinology, and Diabetes, University of Michigan, 1150 W Medical Center Drive, MSRB II, 5570B, Ann Arbor, MI, 48109, USA. aturcu@umich.edu.
Abstract
PURPOSE OF REVIEW: Primary aldosteronism (PA) is the most common cause of secondary hypertension. Emerging evidence suggests that PA is associated with cardiovascular, metabolic, and renal complications, that likely develop insidiously, due to prolonged inappropriate mineralocorticoid receptor activation. In this review, we discuss the expanding clinical and pathological spectrum of PA. RECENT FINDINGS: Clinical and molecular studies conducted over the recent years reveal that PA traverses a series of contiguous stages. Pre-clinical, but hormonally overt PA has been identified in patients with normal blood pressure, and such patients harbor an increased risk of developing hypertension. Similarly, genetic and histopathological advancements have exposed a spectrum of PA pathology that corresponds to a continuum that spans from pre-clinical stages to florid PA. PA evolves from pre-hypertensive stages to resistant hypertension, along with serious cardiovascular and renal consequences. Early recognition of PA and targeted therapy will be essential for cardiovascular morbidity and mortality prevention in a large number of patients.
PURPOSE OF REVIEW: Primary aldosteronism (PA) is the most common cause of secondary hypertension. Emerging evidence suggests that PA is associated with cardiovascular, metabolic, and renal complications, that likely develop insidiously, due to prolonged inappropriate mineralocorticoid receptor activation. In this review, we discuss the expanding clinical and pathological spectrum of PA. RECENT FINDINGS: Clinical and molecular studies conducted over the recent years reveal that PA traverses a series of contiguous stages. Pre-clinical, but hormonally overt PA has been identified in patients with normal blood pressure, and such patients harbor an increased risk of developing hypertension. Similarly, genetic and histopathological advancements have exposed a spectrum of PA pathology that corresponds to a continuum that spans from pre-clinical stages to florid PA. PA evolves from pre-hypertensive stages to resistant hypertension, along with serious cardiovascular and renal consequences. Early recognition of PA and targeted therapy will be essential for cardiovascular morbidity and mortality prevention in a large number of patients.
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