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1 rone:renin ratios (a screening parameter for primary aldosteronism).
2 e approach to the diagnosis and subtyping of primary aldosteronism.
3 the development of new treatment options for primary aldosteronism.
4 tive value for detecting biochemically overt primary aldosteronism.
5 th systems suggests low rates of testing for primary aldosteronism.
6 y 6 hours for 4 days) to diagnose or exclude primary aldosteronism.
7 nd follow-up of adrenalectomy for unilateral primary aldosteronism.
8 ists are the recommended medical therapy for primary aldosteronism.
9 ble way to correctly diagnose the subtype of primary aldosteronism.
10 ng from Cav1.3 hyperactivity, in particular, primary aldosteronism.
11 tension including obstructive sleep apnea or primary aldosteronism.
12 unction Ca(2+) channel mutations in APAs and primary aldosteronism.
13 o renin ratio is a useful screening tool for primary aldosteronism.
14 nsion often persists after adrenalectomy for primary aldosteronism.
15 xpanded extracellular fluid volume, e.g., in primary aldosteronism.
16 t 4 was considered indicative of lateralized primary aldosteronism.
17 isk is observed even in subclinical forms of primary aldosteronism according to studies conducted pri
18 escape phenomenon is clinically relevant as primary aldosteronism affects nearly one in ten hyperten
20 nd follow-up of adrenalectomy for unilateral primary aldosteronism and apply these criteria to an int
21 PAs and has the potential to completely cure primary aldosteronism and hypertension when most of the
25 a previously undescribed syndrome featuring primary aldosteronism and neuromuscular abnormalities.
26 med our understanding of the pathogenesis of primary aldosteronism and of its clinical phenotypes.
27 nin levels, as a confirmatory diagnostic for primary aldosteronism and to quantify the magnitude of r
28 ociations between resistant hypertension and primary aldosteronism and with obstructive sleep apnea.
29 se, which spans subclinical stages to florid primary aldosteronism, and from single-focal or multifoc
30 a detailed insight in the genetic causes of primary aldosteronism, and mineralocorticoid receptor bl
31 uggests that milder and subclinical forms of primary aldosteronism are highly prevalent, yet their co
32 100 patients who underwent adrenalectomy for primary aldosteronism at one tertiary medical center and
34 udy aimed to assess whether early changes in primary aldosteronism biomarkers during young adulthood
35 t diet (relative autonomy, characteristic of primary aldosteronism), but plasma aldosterone was only
36 ssment of patients diagnosed with unilateral primary aldosteronism by adrenal venous sampling who had
38 ues for an orthogonal treatment approach for primary aldosteronism by specifically targeting the inte
43 f mineralocorticoid hypertension is probably primary aldosteronism; controlled posture studies to mea
44 Adrenal tumors driving hormone excess, like primary aldosteronism, Cushing syndrome, and pheochromoc
46 s occur in a handful of conditions including primary aldosteronism, distal renal tubular acidosis, Li
47 of radiofrequency (RF) ablation in treating primary aldosteronism due to aldosterone-producing adeno
54 current practice of MR antagonist therapy in primary aldosteronism is associated with significantly h
57 tion of hypertension after adrenalectomy for primary aldosteronism is independently associated with a
58 l BP, a biochemical phenotype of subclinical primary aldosteronism is negatively associated with card
64 ovascular events was higher in patients with primary aldosteronism on MR antagonists than in patients
65 S1R genes are involved in the development of primary aldosteronism (PA) and hypercortisolism [Cushing
66 pertensive population the true prevalence of primary aldosteronism (PA) and its main subtypes, aldost
70 xcess aldosterone secretion in patients with primary aldosteronism (PA) impairs their cardiovascular
84 nous sampling (AVS) is crucial for subtyping primary aldosteronism (PA) to explore the possibility of
88 igh prevalence and associated complications, primary aldosteronism remains largely under-recognized,
89 clinically relevant spectrum of subclinical primary aldosteronism (renin-independent aldosteronism)
93 This Review discusses how redefining the primary aldosteronism syndrome as a multidimensional spe
96 ous and compensatory diuresis that occurs in primary aldosteronism to correct and rebalance fluid hom
98 We identified 602 eligible patients with primary aldosteronism treated with MR antagonists and 41
99 ident cardiovascular events in patients with primary aldosteronism treated with MR antagonists compar
100 aged 18 years or older, with a diagnosis of primary aldosteronism under the Endocrine Society's crit
105 reatment-resistant hypertension, testing for primary aldosteronism was rare and was associated with h
107 n-independent aldosteronism (ie, subclinical primary aldosteronism), was associated with increased ar
108 prevalence estimates for biochemically overt primary aldosteronism were 11.3% (CI, 5.9% to 16.8%), 15
111 unction mutation is sufficient to cause mild primary aldosteronism, whereas loss of Ca(V)3.2 channel
113 cross-sectional study assessed patients with primary aldosteronism who underwent simultaneous AVS at
114 re for identifying patients with lateralized primary aldosteronism who would benefit from surgery.
115 y clinical study of 677 participants without primary aldosteronism, who were studied on both high and
116 s and mortality was limited to patients with primary aldosteronism whose renin activity remained supp
117 ations for the diagnosis and pathogenesis of primary aldosteronism with and without adrenal hyperplas
118 iscovery that Cav1.3 gain-of-function causes primary aldosteronism with seizures, neurologic abnormal