The hallmark of primary hyperaldosteronism is resistant hypertension. A positive history of spontaneous or unprovoked hypokalemia and treatment-resistant (refractory) hypertension are suggestive of primary hyperaldosteronism. The most common symptoms of primary hyperaldosteronism include headaches, facial flushing, vision changes, and weakness.

Primary hyperaldosteronism may be suspected in the following scenarios:

• Patients with a history of spontaneous or unprovoked hypokalemia along with hypertension.
• Patients who develop severe and/or persistent hypokalemia while on low to moderate doses of potassium-wasting diuretics.
• Patients with a history of treatment-refractory (resistant) hypertension (HTN).

Patients with profound hypokalemia report fatigue, muscle weakness, cramping, headaches, and palpitations. They can also have polydipsia and polyuria from hypokalemia-induced nephrogenic diabetes insipidus. Long-standing HTN may lead to cardiac, retinal, renal, and neurologic problems, with all the associated symptoms and signs. Patients with primary hyperaldosteronism may have subclinical systolic dysfunction, more bradycardia, higher blood pressure, and vascular resistance values than those with the secondary hyperaldosteronism. Plasma renin activity has been found to be lower in primary than in secondary hyperaldosteronism.

Common symptoms of primary hyperaldosteronism (PA) include:^{[1][2][3][4][5][6]}

• Headaches
• Facial flushing
• Weakness
• Visual impairment
• Impaired consciousness
• Seizures (hypertensive encephalopathy)

• Constipation
• Polyuria and polydipsia (because of impaired renal concentrating ability)
• Weakness

Less common symptoms of Conn’s syndrome (primary hyperaldosteronism) include:^[7][8]

• Paralysis
• Palpitations
• Ileus