Familial or Genetic Primary Aldosteronism and Gordon Syndrome

Stowasser, Michael; Pimenta, Eduardo; Gordon, Richard D.

doi:10.1016/j.ecl.2011.01.007

Cited by 26 publications

(12 citation statements)

References 139 publications

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“…Despite the volume overload aldosterone is not suppressed because the elevated potassium can induce its secretion. Plasma potassium is a more reliable measure than serum potassium in this disorder and falsely elevated K+ due to hemolysis can further complicate the confirmation of the disorder (356). Hypercalciuria also occurs.…”

Section: Pseudohypoaldosteronism Typementioning

confidence: 98%

“…Salt restriction is effective in normalizing potassium concentrations in some individuals with the disorder (356). The disorder is notable in that thiazide diuretics ameliorate the clinical abnormalities of the syndrome remarkably well.…”

Section: Pseudohypoaldosteronism Typementioning

confidence: 98%

“…In PHA2, plasma renin activity is suppressed and the aldosterone concentration can range from the low normal to the high normal range (120,356). Despite the volume overload aldosterone is not suppressed because the elevated potassium can induce its secretion.…”

Section: Pseudohypoaldosteronism Typementioning

confidence: 98%

“…The most severe forms of the disease may additionally have features of short stature, muscle weakness, and cognitive impairment (120). Males develop hypertension more often than women and have more significant elevation in BP as a rule (356).…”

Section: Pseudohypoaldosteronism Typementioning

confidence: 99%

“…The disorder is notable in that thiazide diuretics ameliorate the clinical abnormalities of the syndrome remarkably well. Typically, the initial dose of the thiazide should be 50% of a standard dose used to treat subjects with essential hypertension (356). Patients treated with a low dose of hydrochlorothiazide or chlorthalidone can have effective and stable control of BP for decades.…”

Section: Pseudohypoaldosteronism Typementioning

confidence: 99%

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Pathophysiology, Diagnosis, and Treatment of Mineralocorticoid Disorders

Magill

2014

Comprehensive Physiology

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The renin-angiotensin-aldosterone system (RAAS) is a major regulator of blood pressure control, fluid, and electrolyte balance in humans. Chronic activation of mineralocorticoid production leads to dysregulation of the cardiovascular system and to hypertension. The key mineralocorticoid is aldosterone. Hyperaldosteronism causes sodium and fluid retention in the kidney. Combined with the actions of angiotensin II, chronic elevation in aldosterone leads to detrimental effects in the vasculature, heart, and brain. The adverse effects of excess aldosterone are heavily dependent on increased dietary salt intake as has been demonstrated in animal models and in humans. Hypertension develops due to complex genetic influences combined with environmental factors. In the last two decades, primary aldosteronism has been found to occur in 5% to 13% of subjects with hypertension. In addition, patients with hyperaldosteronism have more end organ manifestations such as left ventricular hypertrophy and have significant cardiovascular complications including higher rates of heart failure and atrial fibrillation compared to similarly matched patients with essential hypertension. The pathophysiology, diagnosis, and treatment of primary aldosteronism will be extensively reviewed. There are many pitfalls in the diagnosis and confirmation of the disorder that will be discussed. Other rare forms of hyper- and hypo-aldosteronism and unusual disorders of hypertension will also be reviewed in this article.

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Section: Pseudohypoaldosteronism Typementioning

confidence: 98%

Section: Pseudohypoaldosteronism Typementioning

confidence: 98%

Section: Pseudohypoaldosteronism Typementioning

confidence: 98%

Section: Pseudohypoaldosteronism Typementioning

confidence: 99%

Section: Pseudohypoaldosteronism Typementioning

confidence: 99%

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