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1 hy, whereas gain-of-function mutations cause hyperaldosteronism.
2 herapeutic value for curbing HF-exacerbating hyperaldosteronism.
3 l conditions characterized and aggravated by hyperaldosteronism.
4 as a possible therapeutic target for primary hyperaldosteronism.
5 ockout mice exhibit the hallmarks of primary hyperaldosteronism.
6 cluding a large, undiagnosed pool of primary hyperaldosteronism.
7 iagnosis and estimated prevalence of primary hyperaldosteronism.
8 .0001) compared with the 44 subjects without hyperaldosteronism.
9 n promoting hypertension in conjunction with hyperaldosteronism.
10 d gene that causes glucocorticoid-remediable hyperaldosteronism.
11 c alkalosis with normotensive hyperreninemic hyperaldosteronism.
12  related to deteriorating liver function and hyperaldosteronism.
13 -producing adenomas of patients with primary hyperaldosteronism.
14  was significantly lower in 36 subjects with hyperaldosteronism (1.8+/-1.3% versus 3.9+/-1.9% from ba
15 ma who only presented with clinical signs of hyperaldosteronism after renal transplantation.
16 iagnosis and treatment can provide a cure of hyperaldosteronism and hypertension, even when the latte
17 sh an animal model of nontumorigenic primary hyperaldosteronism and identify TASK channels as a possi
18               An association between chronic hyperaldosteronism and medullary nephrocalcinosis has ra
19 hat support our proposed association between hyperaldosteronism and nephrocalcinosis.
20 ontributes to hypertension in both classical hyperaldosteronism and obesity-associated hypertension.
21 of, and differentiation of causes of primary hyperaldosteronism and the Cushing syndrome.
22  tissue calcification, volume depletion with hyperaldosteronism, and early death.
23 s included hyperphosphatemia, hypercalcemia, hyperaldosteronism, and elevated levels of 1,25-dihydrox
24 th deficits, rapid aging, hyperphosphatemia, hyperaldosteronism, and extensive vascular and soft tiss
25 dohypoaldosteronism, including hyperkalemia, hyperaldosteronism, and metabolic acidosis.
26 ars (range 28-69 years) diagnosed as primary hyperaldosteronism, and who underwent AVS from January 2
27  demonstrated significant suppression of the hyperaldosteronism as well as marked attenuation of prot
28 enic by a novel mechanism in which secondary hyperaldosteronism, associated with an adrenal-specific
29                  It is hypothesized that the hyperaldosteronism attending this model stems from the c
30 is not limited to patients with demonstrable hyperaldosteronism but instead can be effective in resis
31  Yet, the etiology of nontumorigenic primary hyperaldosteronism caused by bilateral idiopathic hypera
32                                              Hyperaldosteronism causes endothelial dysfunction indepe
33                        Primary and secondary hyperaldosteronism correlate with LV enlargement and hig
34                                              Hyperaldosteronism correlates positively with vascular r
35                  The importance of K for the hyperaldosteronism during dietary Na restriction was ver
36  angiotensin, led to a marked attenuation of hyperaldosteronism during dietary Na restriction.
37 otensin-independent mechanism exists for the hyperaldosteronism during LS; (b) high K is a central co
38 xia-PAH rats and monocrotaline-PAH rats with hyperaldosteronism expressed increased levels of the Rap
39 prior to adrenalectomy for all patients with hyperaldosteronism; however, cross-sectional imaging res
40 rs cause endocrine diseases (such as primary hyperaldosteronism, hypercortisolism, hyperandrogenism,
41  normally, intermediary feedback signals for hyperaldosteronism, i.e., both hypotension and high K, a
42 Na(+) depletion was used to induce secondary hyperaldosteronism in rats, or aldosterone was administe
43 terone synthesis; in systemic blood vessels, hyperaldosteronism induces vascular dysfunction by incre
44                                      Primary hyperaldosteronism is a well-recognized cause of seconda
45                                      Primary hyperaldosteronism is an uncommon cause of hypertension
46                                              Hyperaldosteronism is associated with impaired endotheli
47                                      Indeed, hyperaldosteronism is associated with impaired pancreati
48                                              Hyperaldosteronism is associated with impaired vascular
49                              Obesity-induced hyperaldosteronism is independent of the known regulator
50                                              Hyperaldosteronism leads todeleterious effects on the ki
51  been described: glucocorticoid-suppressible hyperaldosteronism, Liddle's syndrome, and apparent mine
52 ess aldosterone production, individuals with hyperaldosteronism lose this regulation, leading to a st
53                            Previously silent hyperaldosteronism may be unmasked by a successful renal
54 ynthesis seen in glucocorticoid-suppressible hyperaldosteronism may cause hypokalemia, suppressed pla
55                                 Importantly, hyperaldosteronism occurred independently of the renin-a
56                                              Hyperaldosteronism occurs independently of angiotensin I
57  inflammasome, suggesting that the effect of hyperaldosteronism on the inflammasome may be mediated t
58                   Hypertensive patients with hyperaldosteronism or normal levels of aldosterone exhib
59 result differs from that expected in primary hyperaldosteronism, our finding argues against low-renin
60 rved in Kiss1-/- females corrected overtime, hyperaldosteronism persisted at 14 months and correlated
61 emission tomography in patients with primary hyperaldosteronism (PHA).
62 aldosteronism caused by bilateral idiopathic hyperaldosteronism remains unknown.
63 cal success rates of surgery for the cure of hyperaldosteronism secondary to aldosterone-producing ad
64                     We conclude that chronic hyperaldosteronism should be included as one of the caus
65                                              Hyperaldosteronism sustains much of the hypertension, bu
66 ednisone to reduce the symptoms of secondary hyperaldosteronism that can occur with AA monotherapy.
67 rovides an inducible and reversible model of hyperaldosteronism to investigate PA therapeutics and th
68            Here we describe three women with hyperaldosteronism, two who presented in pregnancy and o
69  Ca(V)3.2) cause autosomal-dominant familial hyperaldosteronism type IV (FH-IV) and early-onset hyper
70 ermline mutations in ion channels in primary hyperaldosteronism underscores the importance of plasma
71                                              Hyperaldosteronism was diagnosed on the basis of a renin
72 ng diagnostic evaluation of 26 patients with hyperaldosteronism, we administered adrenocorticotrophic
73 ared with unilateral lesions, while rates of hyperaldosteronism were similar in both groups (4.3% [1
74 de may offer a novel way of treating primary hyperaldosteronism, which avoids the vascular side effec
75 67 years; median age, 46 years) with primary hyperaldosteronism who underwent 1.5-T MR imaging betwee
76                    We describe five cases of hyperaldosteronism with a long- standing history in whom
77  tubular disorder characterized by secondary hyperaldosteronism with hypokalemic and hypochloremic me