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Primary aldosteronism

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  • Part 1 book "Kaplan’s clinical hypertension" includes content: Hypertensive crises, renal parenchymal hypertension, renovascular hypertension, primary aldosteronism, pheochromocytoma (with a preface about incidental adrenal masses), hypertension induced by cortisol or deoxycorticosterone, other forms of identifiable hypertension, hypertension with pregnancy and the pill, hypertension in childhood and adolescence.

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  • Adrenocortical adenomas (ACAs) can lead to the autonomous secretion of aldosterone responsible for primary aldosteronism (PA), which is the most common form of secondary arterial hypertension. However, the authentic fundamental mechanisms underlying ACAs remain unclear.

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  • Glomerular hyperfiltration has been recently noticed as an important issue in primary aldosteronism (PA) patients. However, its effect on the cardiovascular system remains unknown.

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  • Metabolic Alkalosis Associated with ECFV Expansion, Hypertension, and HyperaIncreased aldosterone levels may be the result of autonomous primary adrenal overproduction or of secondary aldosterone release due to renal overproduction of renin. Mineralocorticoid excess increases net acid excretion and may result in metabolic alkalosis, which may be worsened by associated K + deficiency. ECFV expansion from salt retention causes hypertension.

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  • Differential Diagnosis To establish the cause of metabolic alkalosis (Table 48-6), it is necessary to assess the status of the extracellular fluid volume (ECFV), the recumbent and upright blood pressure, the serum [K+], and the renin-aldosterone system. For example, the presence of chronic hypertension and chronic hypokalemia in an alkalotic patient suggests either mineralocorticoid excess or that the hypertensive patient is receiving diuretics.

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  • Decreased aldosterone synthesis may be due to primary adrenal insufficiency (Addison's disease) or congenital adrenal enzyme deficiency (Chap. 336). Heparin (including low-molecular-weight heparin) inhibits production of aldosterone by the cells of the zona glomerulosa and can lead to severe hyperkalemia in a subset of patients with underlying renal disease, diabetes mellitus, or those receiving K+-sparing diuretics, ACE inhibitors, or NSAIDs.

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