Clinical Presentation of Hyperaldosteronism

The clinical presentation of hyperaldosteronism varies by case and ranges from asymptomatic to mild to severe symptoms including hypertension, hypokalemia, nausea, fatigue, headache, edema, hyperactive deep tendon reflexes, paresthesia, numbness, and muscle weakness.2 The most common presentation of aldosteronism is normokalemic hypertension; thus, hypokalemia is no longer a prerequisite for aldosteronism screening.8,9  

Patients who have hypertension secondary to primary aldosteronism tend to have a lower level of hypokalemia compared with patients who have essential hypertension. In one study, the mean serum potassium level in patients with primary aldosteronism was low-normal at 3.74 mmol/L whereas patients with essential hypertension had levels that were, on average, 0.6 mmol/L higher.8,10 The low levels of potassium seen in more severe cases of aldosteronism can cause diminished deep tendon reflexes, cramping, and generalized weakness. Aldosteronism can also cause polyuria and polydipsia presenting similarly to diabetes insipidus and arrhythmia experienced as episodic palpitations.2

Diagnosis of Aldosteronism

Diagnosis of aldosteronism is a 2-step process: the hormone imbalance must first be recognized and then differentiated as a primary or secondary condition. The Endocrine Society recommends measuring ARR to detect possible cases of primary aldosteronism in patients with hypertension and risk factors for aldosteronism (Table).9

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Table. Risk Factors for Primary Aldosteronism9

Sustained BP >150/100 mm Hg on 3 measurements obtained on different days
Hypertension (BP >140/90 mm Hg) resistant to 3 conventional antihypertensive drugs (including a diuretic)
Controlled BP (<140/90 mm Hg) on ≥4 antihypertensive drugs
Hypertension and spontaneous or diuretic-induced hypokalemia
Hypertension and adrenal incidentaloma
Hypertension and sleep apnea
Hypertension and a family history of early-onset hypertension or cerebrovascular accident at a young age (<40 years)
Hypertensive first-degree relatives of patients with PA
BP, blood pressure

Patients with a positive ARR should undergo 1 or more confirmatory tests; however, patients with spontaneous hypokalemia, undetectable renin, and plasma renin activity (PAC) more than 20 ng/dL (550 pmol/L) do not require confirmatory testing.9 Once a primary pathology is determined, adrenal computed tomography (CT) is typically used to determine if the patient has adrenocortical carcinoma, to differentiate between unilateral and bilateral adrenal disease, and to assist with surgical planning when appropriate.9 The Endocrine Society recommends using CT in conjunction with adrenal venous sampling, which is an invasive bilateral blood draw used to compare hormone production from each gland and differentiate between unilateral vs bilateral pathology.3,9

Complications of Aldosteronism

Severe complications of aldosteronism include neuromuscular pain or weakness and retinopathy, which are usually the result of extreme hypokalemia and uncontrolled hypertension. These conditions are avoidable and underscore the importance of continuous monitoring of electrolyte levels and blood pressure control. Patients with primary aldosteronism and treatmeant-resistant hypertension are more likely to develop chronic kidney disease compared with patients with essential hypertension.8,11

Hypersecretion of aldosterone can cause diffuse organ damage even before the patient is symptomatic.6 Death from cardiovascular causes is more common in patients with primary aldosteronism than in patients with essential hypertension.6 Even in asymptomatic patients with blood pressure within normal limits, there has been evidence of left ventricular hypertrophy and fibrosis of cardiac tissue.6 This is due to the presence d receptors in cardiac tissue and the effect of increased aldosterone binding as a result of adrenal hypersecretion.6 The mineralocorticoid receptors present in cardiac tissue allow aldosterone to regulate hypertrophy of cardiac soft tissue. This is why excessive binding to these receptors in patients with aldosteronism can lead to complications of cardiac muscle hypertrophy and vascular smooth muscle hypertrophy with the potential for heart failure and death.2,6   

This article originally appeared on Clinical Advisor