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Secondary Arterial Hypertension


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

The kidney plays a fundamental role in blood pressure regulation by modulating blood volume through filtration and fluid reabsorption and by 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. The latter is then transformed into angiotensin II by the angiotensin-converting enzyme (ACE), a key target of antihypertensive therapy.
Most cases of secondary hypertension have a renal origin, with the most common cause being renal artery stenosis, usually due to atherosclerotic plaques or, more rarely, fibromuscular dysplasia. Even unilateral renal artery stenosis can activate the RAAS, leading to hypertension.
In addition to renal artery stenosis, all renal conditions that reduce glomerular filtration can cause arterial hypertension through RAAS activation.

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

In secondary hypertension, elevated blood pressure values represent a symptom of a broader clinical picture linked to the underlying disease.
The treatment of secondary arterial hypertension involves controlling blood pressure levels to prevent acute complications and, most importantly, addressing the underlying disease. If the causative condition is treated, hypertension may also resolve.
In secondary hypertension, signs and symptoms are similar to those of primary hypertension but occur within a broader syndrome related to the underlying pathology.
Complications and target organ effects are also similar, particularly acute complications caused by sudden and significant blood pressure increases.
Chronic complications, on the other hand, take years to develop; therefore, if the underlying disease is treated promptly, they can be prevented.
    References
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