What is secondary arterial hypertension?

Secondary arterial hypertension is a form of hypertension caused by an identifiable disease, most frequently of renal or endocrine origin.

What are the main causes of secondary arterial hypertension?

The main causes include renal artery stenosis, chronic kidney diseases, hyperaldosteronism, pheochromocytoma, hyperthyroidism, Cushing's syndrome, and renin-secreting tumors.

When should secondary hypertension be suspected?

Secondary hypertension should be suspected in young patients, treatment-resistant cases, or when specific clinical signs related to the underlying disease are present.

Which tests are useful for diagnosing secondary arterial hypertension?

Useful tests include blood chemistry and hormone assays, renal and renal artery imaging (ultrasound, CT/MR angiography), ambulatory blood pressure monitoring, and urine tests.

What complications are associated with secondary arterial hypertension?

Complications include hypertensive crises, acute kidney injury, stroke, myocardial infarction, heart failure, and hypertensive retinopathy.

How is secondary arterial hypertension treated?

Management involves treating the primary cause and controlling blood pressure with targeted antihypertensive drugs.

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Secondary Arterial Hypertension

Article written and reviewed by Dr Luca Moretti

Secondary arterial hypertension is defined as a chronic elevation of blood pressure above 140 mmHg systolic and 90 mmHg diastolic, attributable to an identifiable specific cause.
Secondary arterial hypertension can result from pathological conditions that increase peripheral vascular resistance, cardiac output, or blood volume, thereby altering systemic pressure balance.

The kidney plays a fundamental role in blood pressure regulation by modulating blood volume through filtration and reabsorption of fluids and regulating the renin-angiotensin-aldosterone system (RAAS).
In response to hypovolemia or hypotension, the kidney secretes renin, which catalyzes the conversion of angiotensinogen into angiotensin I. Angiotensin I is then converted to angiotensin II by the angiotensin-converting enzyme (ACE), a key target of antihypertensive therapy.
Most secondary hypertensions have a renal origin, the most common being renal artery stenosis, often due to atherosclerotic plaques or, more rarely, fibromuscular dysplasia. Even unilateral renal artery stenosis can activate RAAS, causing hypertension.
Beyond renal artery stenosis, all renal diseases that reduce glomerular filtration rate can cause arterial hypertension through activation of the RAAS.

Blood pressure control is also influenced by endocrine factors through secretion of hormones with vasopressor and/or positive inotropic effects on the heart:

Pheochromocytoma: excess adrenaline and noradrenaline
Hyperthyroidism: excess FT3 and FT4
Hyperaldosteronism: excess aldosterone
Cushing’s Syndrome: excess cortisol
Hyperparathyroidism: excess parathyroid hormone acting indirectly by causing hypercalcemia which can induce arteriolar vasoconstriction and renal damage, contributing to secondary hypertension.
Hyperreninemia: excess renin caused by renin-secreting endocrine tumors, a rare condition.

In secondary hypertension, elevated blood pressure values represent a symptom of a broader clinical picture related to the underlying pathology.
Treatment of secondary arterial hypertension involves controlling blood pressure to prevent acute complications and, most importantly, therapy of the underlying disease. If the triggering cause is treated, hypertension may also resolve.
In secondary hypertensions, signs and symptoms overlap with those of primary hypertension but occur within a broader syndrome linked to the underlying disease.
Complications and effects on target organs are also similar, particularly acute ones related to sudden and significant blood pressure increases.
Chronic complications require years to manifest; therefore, timely treatment of the underlying pathology can prevent them.

References

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