In patients with cirrhosis and ascites, the reduction in circulating fluid volume leads to decreased perfusion through the kidneys and results in increased aldosterone secretion. In left-sided congestive heart failure and cor pulmonale, a decrease in cardiac output leads to aldosterone stimulation. Renal artery stenosis (atherosclerosis or fibromuscular dysplasia) causes decreased blood flow through the kidneys, simulates a false sense of hypovolemia, and activates aldosterone secretion. It can happen due to physiologic state of transient RAAS activation such as hypovolemia but can be seen in pathological states of sustained RAAS activation. Secondary hyperaldosteronism (SHA) occurs due to the excess stimulation of the RAAS. These patients are usually asymptomatic but can typically present with hypertension and hypokalemia. In the remaining one-third of patients, a tumor in the zona glomerulosa, known as Conn syndrome, can directly cause an increase in aldosterone. The most common cause of PHA (in two-thirds of the patients) is idiopathic bilateral adrenal hyperplasia. Primary hyperaldosteronism (PHA) occurs due to the excess aldosterone production by the adrenal gland.
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