Conn first described the syndrome associated with primary secretion of excessive amounts of aldosterone.


Pathologic causes include:

(1) bilateral adrenal hyperplasia

(2) unilateral adrenal hyperplasia

(3) adrenal adenoma

(4) adrenocortical carcinoma

(5) familial hypertension (FH), Types I or II

(6) paraneoplastic ectopic tumor production


Clinical findings:

(1) hypertension, typically resistant to therapy

(2) weakness, cramps or tetany (secondary to hypokalemia)

(3) polyuria and nocturia (secondary to hypokalemia)


Some patients may be asymptomatic.


Laboratory findings:

(1) hypokalemia

(2) elevated urinary potassium excretion

(3) sodium retention

(4) low serum plasma renin activity

(5) increased plasma aldosterone activity

(6) elevated ratio of plasma aldosterone to renin activity

(7) variable hyperglycemia

(8) variable proteinuria


The elevated aldosterone production is not suppressed by oral sodium loading.


Confirmatory tests:

(1) 4-hour intravenous sodium loading test

(2) 4-day fludrocortisone administration


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