ライフサイエンスコーパス: aldosteronism

1 w-up of adrenalectomy for unilateral primary aldosteronism.

2 the recommended medical therapy for primary aldosteronism.

3 to correctly diagnose the subtype of primary aldosteronism.

4 Cav1.3 hyperactivity, in particular, primary aldosteronism.

5 including obstructive sleep apnea or primary aldosteronism.

6 Ca(2+) channel mutations in APAs and primary aldosteronism.

7 ratio is a useful screening tool for primary aldosteronism.

8 ten persists after adrenalectomy for primary aldosteronism.

9 extracellular fluid volume, e.g., in primary aldosteronism.

10 s for 4 days) to diagnose or exclude primary aldosteronism.

11 Patients with primary aldosteronism also had higher adjusted risks for inciden

12 finding parallels an age-related autonomous aldosteronism and abnormal aldosterone physiology that p

13 w-up of adrenalectomy for unilateral primary aldosteronism and apply these criteria to an internation

14 These individuals had severe progressive aldosteronism and hyperplasia requiring bilateral adrena

15 immunostimulatory state that appears during aldosteronism and leads to a proinflammatory coronary va

16 Classical primary aldosteronism and lesser degrees of aldosterone excess,

17 Glucocorticoid-suppressible aldosteronism and Liddle's syndrome, each inherited as a

18 +) conductance in a Mendelian form of severe aldosteronism and massive bilateral adrenal hyperplasia.

19 Until the true prevalence of primary aldosteronism and monogenic forms of mineralocorticoid h

20 ously undescribed syndrome featuring primary aldosteronism and neuromuscular abnormalities.

21 s between resistant hypertension and primary aldosteronism and with obstructive sleep apnea.

22 led insight in the genetic causes of primary aldosteronism, and mineralocorticoid receptor blockers h

23 ents who underwent adrenalectomy for primary aldosteronism at one tertiary medical center and was ext

24 f patients diagnosed with unilateral primary aldosteronism by adrenal venous sampling who had undergo

25 ed subjects with hypertension due to primary aldosteronism by age 10.

26 In aldosteronism, Ca2+ and Mg2+ losses lead to a fall in [C

27 Primary aldosteronism comprises subtypes that need different the

28 locorticoid hypertension is probably primary aldosteronism; controlled posture studies to measure pla

29 in a handful of conditions including primary aldosteronism, distal renal tubular acidosis, Liddle's d

30 ofrequency (RF) ablation in treating primary aldosteronism due to aldosterone-producing adenoma (APA)

31 Aldosteronism eventuates in a proinflammatory/fibrogenic

32 In aldosteronism, hypercalciuria and hypermagnesuria and ac

33 tricular dysfunction caused by chronic hyper-aldosteronism in vivo is completely prevented in cardiac

34 adrenocortical cell mass and the severity of aldosteronism in vivo, accounting for the milder phenoty

35 accompanies excretory Ca2+ losses induced by aldosteronism in which elevated parathyroid hormone leve

36 We present an interesting case of primary aldosteronism in which planar scintigraphy and SPECT wer

37 cal primary aldosteronism (renin-independent aldosteronism) in normotension.

38 Neurohormonal activation, including aldosteronism, in HF and RHT, has provided the pathophys

39 Primary aldosteronism is a potentially curable cause of hyperten

40 g2+ excretion and bone loss that accompanies aldosteronism is aggravated with furosemide and is atten

41 Thus, aldosteronism is associated with an activation of circul

42 Hyper-aldosteronism is associated with myocardial dysfunction

43 practice of MR antagonist therapy in primary aldosteronism is associated with significantly higher ri

44 Primary aldosteronism is common among patients with resistant hy

45 hypertension after adrenalectomy for primary aldosteronism is independently associated with a lack of

46 Primary aldosteronism is recognized as a severe form of renin-in

47 Primary aldosteronism is the most common curable cause of second

48 Although unilateral primary aldosteronism is the most common surgically correctable

49 Aldosteronism may account for oxi/nitrosative stress, a

50 These results suggest that chronic aldosteronism may have a blood pressure-independent effe

51 rs of four kindreds with early onset primary aldosteronism of unknown cause.

52 r events was higher in patients with primary aldosteronism on MR antagonists than in patients with es

53 ve population the true prevalence of primary aldosteronism (PA) and its main subtypes, aldosterone-pr

54 Primary aldosteronism (PA) causes excess left ventricular (LV) h

55 dosterone secretion in patients with primary aldosteronism (PA) impairs their cardiovascular system.

56 Primary aldosteronism (PA) is a common and underdiagnosed diseas

57 Primary aldosteronism (PA) is common and associates with excess

58 Primary aldosteronism (PA) is the most common cause of secondary

59 drenocortical hormone excess, due to primary aldosteronism (PA) or hypercortisolemia, causes hyperten

60 logical treatments on outcomes among primary aldosteronism (PA) patients.

61 Primary aldosteronism (PA) represents the most common cause of s

62 o localize aldosterone production in primary aldosteronism (PA).

63 lly relevant spectrum of subclinical primary aldosteronism (renin-independent aldosteronism) in normo

64 he juxtaglomerular apparatus of the kidneys, aldosteronism resulting from adrenal cortical hyperplasi

65 of the hypertension of Kcnmb1(-/-) is due to aldosteronism, resulting from renal potassium retention

66 ction; whether this occurs also in secondary aldosteronism (SA) without hypertension is unknown.

67 Screening for primary aldosteronism should nonetheless be done in every indivi

68 In rats with aldosteronism, spironolactone preserves skeletal strengt

69 The Primary Aldosteronism Surgical Outcome (PASO) study was an inter

70 a spectrum of subclinical renin-independent aldosteronism that increases risk for hypertension exist

71 gnized as a severe form of renin-independent aldosteronism that results in excessive mineralocorticoi

72 iddle syndrome and glucocorticoid-remediable aldosteronism, the abundance of plausible candidate gene

73 dentified 602 eligible patients with primary aldosteronism treated with MR antagonists and 41 853 age

74 rdiovascular events in patients with primary aldosteronism treated with MR antagonists compared with

75 We identified patients with primary aldosteronism using International Classification of Dise

76 Primary aldosteronism was confirmed by using the oral sodium-loa

77 At 3-month follow-up, primary aldosteronism was resolved in 33 (92%) patients, with a

78 al study of 677 participants without primary aldosteronism, who were studied on both high and restric

79 rtality was limited to patients with primary aldosteronism whose renin activity remained suppressed (

80 or the diagnosis and pathogenesis of primary aldosteronism with and without adrenal hyperplasia.

81 that Cav1.3 gain-of-function causes primary aldosteronism with seizures, neurologic abnormalities, a