History and exam

Key diagnostic factors

common

hypertension

Any degree of severity and duration. A family history of hypertension was once thought to make a treatable cause less likely, but now, because of familial hyperaldosteronism type II, it makes PA more likely.

May be of early onset in familial hyperaldosteronism types I, II, III, and IV.[16][17]​​[20][21][47][48][105]​​

uncommon

presence of risk factors

Risk factors include: family history of primary aldosteronism and family history of early onset (e.g., <40 years) hypertension and/or stroke.

Other diagnostic factors

common

age 20 to 70 years

Most commonly occurs in adults aged 20 to 70 years, but occasionally diagnosed in children (familial hyperaldosteronism types I, II, III, and IV but rarely other forms) and older adults.​[7][104]

nocturia, polyuria

Whether or not hypokalaemic.[7]

lethargy

Whether or not hypokalaemic.

mood disturbance (irritability, anxiety, depression)

Whether or not hypokalaemic.

difficulty concentrating

Whether or not hypokalaemic.

uncommon

paraesthesias, muscle cramps

If hypokalaemic.[56]

muscle weakness

If hypokalaemic.[56]

palpitations

If hypokalaemic.[56]

Risk factors

strong

family history of PA

There are at least 4 familial forms of primary aldosteronism (PA). An autosomal dominant pattern of inheritance is seen in familial hyperaldosteronism type I (FH-I), familial hyperaldosteronism type II (FH-II), familial hyperaldosteronism type III (FH-III), and familial hyperaldosteronism type IV (FH-IV).[4][13][22][47][48]

FH-I, FH-II, FH-III, and FH-IV all appear to be rare (<1% of PA cases), but FH-I is currently the most commonly reported amongst these entities. The percentage of cases of familial hyperaldosteronism for which the underlying genetic basis has yet to be elucidated is around 6%, but the precise prevalence for each causative mutation will remain uncertain until these are identified, permitting genetic detection of affected individuals.[69] 

The fact that patients with familial hyperaldosteronism of indeterminate genetic origin are clinically indistinguishable from those with apparently sporadic PA (which accounts for 5% to 10% of referred hypertensive patients) raises the possibility that mutations underlying PA in these families may account for a substantial proportion of PA cases in general.[4][13][22]

family history of early onset of hypertension and/or stroke

In familial hyperaldosteronism type I (FH-I), II (FH-II), III (FH-III), and IV (FH-IV), hypertension can be of early onset (e.g., <40 years of age) and in FH-I FH-III may be severe enough to cause early stroke (usually of the haemorrhagic variety).[17][20][21]​​[47][48]

However, the prevalence of FH-I to IV among patients presenting in this way, and among their relatives, is unknown.

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