2021
DOI: 10.1016/j.jfma.2021.03.032
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Taiwan mini-frontier of primary aldosteronism: Updating treatment and comorbidities detection

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Cited by 6 publications
(2 citation statements)
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“…Our study provides clinical implications. Several expert panels suggest that posttreatment PRA is a potential target parameter for MRA titration and reversing renin suppression (ie, ≥1.0 ng/mL per hour) could be a cornerstone of an optimal medical treatment for PA. 1,2,39 These perspectives are based on 4 previous studies, [9][10][11]13 including 2 studies indicating that medically treated patients with PA with posttreatment PRA of ≥1.0 ng/mL per hour potentially have lower incidence risks of CVD, atrial fibrillation, and death compared with those with posttreatment PRA of <1.0 ng/mL per hour. 9,10 The other 2 studies evaluated the association of posttreatment renin status with renal outcomes; however, these studies did not reveal the preferable renal outcomes for medically treated patients with PA with posttreatment PRA ≥1.0 ng/mL per hour than those with posttreatment PRA <1.0 ng/mL per hour.…”
Section: Original Articlementioning
confidence: 99%
“…Our study provides clinical implications. Several expert panels suggest that posttreatment PRA is a potential target parameter for MRA titration and reversing renin suppression (ie, ≥1.0 ng/mL per hour) could be a cornerstone of an optimal medical treatment for PA. 1,2,39 These perspectives are based on 4 previous studies, [9][10][11]13 including 2 studies indicating that medically treated patients with PA with posttreatment PRA of ≥1.0 ng/mL per hour potentially have lower incidence risks of CVD, atrial fibrillation, and death compared with those with posttreatment PRA of <1.0 ng/mL per hour. 9,10 The other 2 studies evaluated the association of posttreatment renin status with renal outcomes; however, these studies did not reveal the preferable renal outcomes for medically treated patients with PA with posttreatment PRA ≥1.0 ng/mL per hour than those with posttreatment PRA <1.0 ng/mL per hour.…”
Section: Original Articlementioning
confidence: 99%
“…Primary aldosteronism (PA) is a genetic condition with continuous, autonomous excessive production of aldosterone and is the most common cause of secondary hypertension. The excess aldosterone causes mineralocorticoid hypertension (14). There have been courses of normotensive pregnancies followed by postpartum hypertension, further diagnosed as PA (15).…”
Section: Primary Hyperaldosteronismmentioning
confidence: 99%