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Secondary hypertension

Secondary hypertension is high blood pressure caused by an underlying medical condition, distinguishing it from primary hypertension, which has no identifiable cause.^[1] It accounts for approximately 10% of hypertension cases in adults, though this prevalence rises to 70-85% in children under 12 years and around 17% in adults aged 65 or older.^[2] This form of hypertension often develops suddenly, tends to cause higher blood pressure levels (such as systolic readings over 180 mm Hg or diastolic over 120 mm Hg), and may be resistant to standard treatments.^[1] Common causes include: Like primary hypertension, secondary hypertension is typically asymptomatic until complications arise, though signs of the underlying condition—such as hypokalemia from aldosteronism or snoring from sleep apnea—may prompt evaluation.^[1] Individuals with sudden-onset hypertension before age 30, after age 55, or with resistant readings should seek medical attention promptly.^[1] Diagnosis involves a detailed history, physical exam, and targeted screening, such as aldosterone-to-renin ratio for primary aldosteronism, renal ultrasound for parenchymal disease, or polysomnography for sleep apnea.^[2]^[3] Management prioritizes treating the root cause—for instance, surgery for unilateral aldosteronism or continuous positive airway pressure for sleep apnea—combined with blood pressure control through lifestyle changes and medications.^[3] Early intervention can reverse end-organ damage and improve long-term outcomes.^[2]

Introduction

Definition and characteristics

Secondary hypertension is defined as elevated blood pressure of ≥130/80 mmHg, as per the 2025 American Heart Association/American College of Cardiology (AHA/ACC) guidelines, resulting from an identifiable underlying medical condition rather than multifactorial idiopathic mechanisms.^[4] This form accounts for approximately 5-10% of hypertension cases among adults, distinguishing it from primary (essential) hypertension, which predominates in 90-95% of instances.^[5] Key characteristics include an onset typically before age 30 years or abruptly after age 55 years, often presenting with severe elevations (stage 2 or higher) that are resistant to three or more antihypertensive agents at optimal doses.^[1]^[6] Patients may exhibit end-organ damage, such as retinopathy or left ventricular hypertrophy, that appears disproportionate to the known duration of hypertension, and blood pressure control can potentially be achieved or cured by addressing the root cause.^[2] In contrast to the gradual, insidious progression of primary hypertension, secondary forms often show labile readings with diurnal fluctuations or associated symptoms tied to the underlying pathology, like episodic headaches.^[7] The recognition of secondary hypertension traces back to the early 20th century, when links to renal parenchymal disease were established as a distinct etiology separate from essential hypertension's non-specific origins.^[8] This historical distinction underscores its potentially reversible nature, emphasizing the importance of identifying clinical clues for targeted evaluation.

Epidemiology

Secondary hypertension accounts for approximately 5% to 10% of all hypertension cases among adults worldwide, though estimates can range up to 25% in certain populations.^[2] In pediatric populations, secondary causes are far more prevalent, comprising 45% to 85% of hypertension cases in specialized clinics, with up to 80% in some cohorts of children and adolescents.^[9] Among adults with treatment-resistant hypertension, defined as uncontrolled blood pressure despite three or more antihypertensive medications, the prevalence of secondary hypertension rises to 10% to 20%, highlighting its disproportionate burden in this subgroup.^[10] Incidence trends for secondary hypertension have remained relatively stable overall, but specific subtypes show increases linked to rising chronic conditions; for instance, obstructive sleep apnea-related cases have grown alongside the global obesity epidemic, contributing to 25% to 50% of hypertension etiologies in affected individuals.^[10] Recent data from 2023 to 2025 indicate that resistant hypertension, often driven by secondary causes, affects 8.5% to 20% of hypertensive adults in the United States, with stable but persistent public health challenges per updated guidelines.^[10] Demographic factors influence the distribution of secondary hypertension, with renovascular causes more common in males due to higher rates of atherosclerotic renal artery stenosis in older age groups.^[11] Certain renal etiologies, such as parenchymal disease leading to end-stage renal disease, show elevated prevalence in Black populations, who face a fourfold higher risk compared to White populations after age adjustment.^[12] Age-specific patterns include peaks in younger individuals for coarctation of the aorta and in the elderly for renal artery stenosis, underscoring the need for targeted screening across life stages.^[13]^[14] Key risk factors for secondary hypertension include chronic conditions like diabetes, which heightens the likelihood of renal parenchymal disease, and obesity, a major driver of obstructive sleep apnea.^[10] Medication use, such as nonsteroidal anti-inflammatory drugs or oral contraceptives, also contributes to secondary forms.^[2] Socioeconomic disparities exacerbate these risks, with lower-income and less-educated groups experiencing reduced access to screening and higher undiagnosed rates, perpetuating inequities in detection and management.^[15]

Common Causes

Obstructive sleep apnea

Obstructive sleep apnea (OSA) is a leading reversible cause of secondary hypertension, particularly among obese adults, where it accounts for 25-50% of cases. This high prevalence is driven by the close interplay between obesity, a major risk factor for OSA, and the resulting intermittent hypoxia and sympathetic nervous system activation that exacerbate blood pressure elevation. In obese individuals with hypertension, OSA prevalence can reach 70-80%, underscoring its role as a modifiable contributor to resistant or poorly controlled hypertension.^[16] The pathophysiology of OSA-induced hypertension involves recurrent upper airway obstructions during sleep, leading to intermittent hypoxia, hypercapnia, and arousals that trigger acute surges in sympathetic activity. These episodes promote chronic oxidative stress and endothelial dysfunction, impairing vascular relaxation and contributing to sustained arterial stiffness. Additionally, intermittent hypoxia activates the renin-angiotensin-aldosterone system, further elevating blood pressure through increased vasoconstriction and sodium retention, resulting in persistent daytime hypertension that often lacks the normal nocturnal dipping pattern.^[17]^[18]^[19] Clinically, OSA-associated hypertension presents with hallmark features of the sleep disorder, including excessive daytime somnolence, loud snoring, and witnessed apneas or gasping during sleep, alongside resistant hypertension that responds poorly to standard antihypertensive therapy. Patients frequently exhibit non-dipping or reverse dipping blood pressure profiles on ambulatory monitoring, reflecting disrupted circadian rhythms due to nocturnal sympathetic overdrive. These individuals face a 2- to 3-fold increased risk of major cardiovascular events, such as myocardial infarction and stroke, independent of other risk factors. Diagnosis relies on polysomnography, which quantifies severity via the apnea-hypopnea index (AHI), with moderate-to-severe OSA defined as ≥15 events per hour.^[20]^[21]^[22] Recent updates in the 2025 American Heart Association (AHA) guidelines emphasize routine screening for OSA in obese patients with hypertension, particularly those with resistant disease or suggestive symptoms, to identify and address this common secondary cause early and mitigate cardiovascular risks.^[4]^[16]

Renal parenchymal disease

Renal parenchymal disease is the most common cause of secondary hypertension among renal etiologies, accounting for 2% to 5% of all hypertension cases overall.^[23] This category includes intrinsic kidney disorders such as chronic glomerulonephritis, diabetic nephropathy, hypertensive nephrosclerosis, and polycystic kidney disease, where damage to the renal parenchyma impairs kidney function and triggers blood pressure elevation.^[2] The underlying pathophysiology stems from reduced nephron mass due to parenchymal injury, which promotes sodium and water retention, leading to intravascular volume expansion and extracellular fluid overload.^[2] This is compounded by inappropriate activation of the renin-angiotensin-aldosterone system (RAAS), increased sympathetic nervous system activity, and endothelial dysfunction, all contributing to heightened systemic vascular resistance and hypertension.^[24] Hypertension typically emerges when the glomerular filtration rate (GFR) declines below 60 mL/min/1.73 m², corresponding to stage 3 chronic kidney disease, as this threshold marks significant impairment in renal excretory capacity. Clinically, patients often present with proteinuria, peripheral edema, and elevated serum creatinine, indicative of ongoing renal insufficiency.^[2] Hypertension may precede overt renal decline in a substantial proportion of cases, accelerating further kidney damage through glomerular hyperfiltration and sclerosis.^[25] Among specific entities, IgA nephropathy—a leading cause of glomerulonephritis—frequently links to recurrent gross hematuria and progressive proteinuria, with hypertension arising from glomerular inflammation and scarring.^[26] Reflux nephropathy, typically originating in childhood from vesicoureteral reflux, results in focal renal scarring and tubulointerstitial damage, often manifesting as hypertension in young adults alongside recurrent urinary tract infections.^[27] Without intervention, both conditions commonly progress to end-stage renal disease, with up to 20% of IgA nephropathy cases reaching kidney failure within 10 years.^[26] Diagnostic evaluation relies on abnormal urinalysis revealing proteinuria, hematuria, or casts, coupled with a reduced estimated GFR on blood tests, prompting further imaging or biopsy to confirm parenchymal involvement.^[2]

Renovascular hypertension

Renovascular hypertension is a secondary form of hypertension resulting from narrowing or stenosis of one or both renal arteries, which impairs blood flow to the kidneys and triggers compensatory mechanisms that elevate systemic blood pressure. This condition represents approximately 1-5% of all hypertension cases, though estimates vary by population, with higher rates (up to 40%) observed in referral centers for refractory hypertension.^[28] It is more prevalent in specific groups, including younger females affected by fibromuscular dysplasia and older adults, particularly smokers, due to atherosclerotic disease.^[29] Unlike intrinsic renal parenchymal disease, renovascular hypertension arises from extrinsic vascular compression on the kidney, leading to ischemia without primary tissue damage.^[30] The pathophysiology centers on renal artery stenosis causing distal ischemia, which stimulates juxtaglomerular cells to release renin, activating the renin-angiotensin-aldosterone system (RAAS). This results in elevated renin levels, angiotensin II-mediated vasoconstriction, aldosterone-induced sodium and water retention, and subsequent hypertension.^[31] Significant hypertension typically develops with greater than 60% luminal narrowing, progressing to a volume-dependent state in chronic cases; bilateral involvement exacerbates the prognosis by increasing the risk of ischemic nephropathy and end-stage renal disease.^[29] Clinically, renovascular hypertension often manifests as resistant hypertension uncontrolled by three or more antihypertensive medications, alongside features such as an audible abdominal bruit on physical examination, episodes of flash pulmonary edema due to acute left ventricular failure, and rapid deterioration of renal function.^[30] Patients may present with a history of sudden-onset or worsening hypertension, particularly in the context of atherosclerotic risk factors or younger age without typical essential hypertension traits. The primary subtypes are fibromuscular dysplasia and atherosclerotic renal artery stenosis. Fibromuscular dysplasia, a non-inflammatory, non-atherosclerotic vasculopathy, typically shows a characteristic "string-of-beads" appearance on angiography due to multifocal stenoses and aneurysms, predominantly affecting the mid-to-distal renal artery in women aged 15-50 years.^[31] Atherosclerotic stenosis, accounting for about 90% of cases, involves plaque buildup at the ostium or proximal renal artery with greater than 70% narrowing, commonly in older patients (>50 years) with comorbidities like diabetes, hyperlipidemia, and smoking history.^[29] Diagnosis relies on non-invasive screening followed by confirmatory imaging. Captopril renography, a functional test, detects hemodynamically significant stenosis by showing delayed renal uptake after angiotensin-converting enzyme inhibition, with sensitivity around 79% and specificity of 82%.^[31] Duplex ultrasound serves as a first-line anatomic tool, identifying stenosis through elevated peak systolic velocity exceeding 200 cm/s (indicating >60% narrowing) and renal-aortic velocity ratios greater than 3.5.^[29] These approaches help differentiate renovascular causes from other secondary hypertension etiologies in high-risk patients.

Primary aldosteronism

Primary aldosteronism, also known as Conn's syndrome, represents the most common endocrine cause of secondary hypertension, characterized by autonomous overproduction of aldosterone from the adrenal glands. This condition accounts for approximately 5% to 10% of all cases of hypertension, with prevalence rising to 20% or higher among patients with resistant hypertension.^[32]^[33] The excess aldosterone leads to suppression of plasma renin activity, promoting renal sodium retention, volume expansion, and potassium excretion, which collectively drive sustained hypertension.^[34] In most instances, this autonomous production arises from either unilateral aldosterone-producing adenoma or bilateral adrenal hyperplasia of the zona glomerulosa.^[34] Clinically, primary aldosteronism often presents with resistant hypertension that is difficult to control with standard antihypertensive therapy, alongside potential electrolyte disturbances. Hypokalemia occurs in about 30% of cases, though many patients are normokalemic, leading to subtler manifestations such as fatigue, muscle weakness, or palpitations; metabolic alkalosis may also accompany these features due to hydrogen ion loss in the kidneys.^[35] The condition's impact is more pronounced in resistant cases, where cardiovascular risks, including stroke and heart failure, are elevated compared to primary hypertension.^[36] The two primary subtypes are Conn syndrome, caused by a unilateral aldosterone-producing adenoma (accounting for 30% to 40% of cases), and idiopathic bilateral adrenal hyperplasia (comprising about 60%). Diagnosis typically involves screening with the plasma aldosterone-renin ratio, where a ratio greater than 30 (with aldosterone level exceeding 15 ng/dL) suggests the condition, particularly in the absence of interfering medications.^[37]^[38] According to the 2025 Endocrine Society clinical practice guideline, screening via aldosterone-renin ratio is recommended for all patients with resistant hypertension or hypokalemia to facilitate early identification and targeted treatment.^[39]

Drug- and substance-induced hypertension

Drug- and substance-induced hypertension refers to elevated blood pressure resulting from the use of certain medications, supplements, or illicit substances that interfere with normal cardiovascular regulation. This form of secondary hypertension accounts for up to 5% of all hypertension cases and is particularly prevalent in settings of polypharmacy, where multiple drugs may interact to exacerbate blood pressure control.^[2]^[40] The underlying mechanisms vary by agent but commonly involve sodium and fluid retention, sympathetic nervous system activation, or disruption of the renin-angiotensin-aldosterone system (RAAS). For instance, non-steroidal anti-inflammatory drugs (NSAIDs) promote volume retention by inhibiting cyclooxygenase enzymes, which reduces renal prostaglandin synthesis and impairs natriuresis, leading to increased blood volume.^[40] Corticosteroids induce similar effects through mineralocorticoid receptor activation, causing dose-dependent sodium retention and elevated systemic vascular resistance.^[40] Sympathetic activation is a key pathway for stimulants like cocaine and amphetamines, which increase catecholamine release and vasoconstriction, potentially precipitating acute hypertensive crises.^[41] Additionally, licorice consumption interferes with RAAS by inhibiting 11β-hydroxysteroid dehydrogenase, allowing cortisol to bind mineralocorticoid receptors and promote sodium retention.^[40] Common pharmacological agents include NSAIDs such as ibuprofen, which are widely used and can elevate systolic blood pressure by approximately 5 mm Hg in susceptible individuals; oral contraceptives containing estrogen, which enhance angiotensinogen production and thereby increase vascular resistance; and cyclosporine, an immunosuppressant that causes endothelial dysfunction and vascular smooth muscle proliferation.^[41]^[2] Among substances, chronic alcohol excess (≥200 g/week) contributes through sympathetic activation and vascular remodeling, while acute caffeine intake (e.g., 2-3 cups of coffee) transiently raises blood pressure by about 10 mm Hg via adenosine antagonism and vasoconstriction.^[40] Clinically, drug- and substance-induced hypertension is often dose-dependent and reversible upon discontinuation of the offending agent, though the time to normalization varies—typically days to weeks for NSAIDs or corticosteroids, but immediate intervention may be needed for severe cases like cocaine-induced crises, which can lead to end-organ damage.^[2]^[40] The hypertension is usually mild to moderate but can become resistant to standard therapy in polypharmacy scenarios. High-risk groups include the elderly, who are more prone to polypharmacy and salt sensitivity; patients with chronic kidney disease; and athletes using performance-enhancing supplements, such as anabolic steroids, which can mimic corticosteroid effects.^[41] Individuals with preexisting hypertension face amplified risks, underscoring the need for medication reconciliation in evaluation.^[41]

Hypertension in pregnancy

Hypertensive disorders of pregnancy affect 5-10% of all pregnancies worldwide, with gestational hypertension and preeclampsia accounting for the majority of cases that develop after 20 weeks of gestation, representing approximately 70-80% of secondary hypertension in this context.^[42]^[43] These conditions are distinct from chronic hypertension, which predates pregnancy or occurs before 20 weeks, and are primarily driven by pregnancy-specific physiological changes rather than underlying non-obstetric causes.^[43] The pathophysiology of these disorders centers on placental ischemia, which triggers the release of anti-angiogenic factors such as soluble fms-like tyrosine kinase-1 (sFlt-1), leading to systemic endothelial dysfunction, widespread vasospasm, and increased vascular permeability.^[44] In preeclampsia, this cascade results in proteinuria and multi-organ involvement, whereas gestational hypertension typically presents without proteinuria or significant end-organ damage.^[45] The imbalance between pro- and anti-angiogenic factors disrupts normal vascular adaptation to pregnancy, contributing to the hallmark hypertension observed after 20 weeks.^[46] Hypertensive disorders in pregnancy are classified into gestational hypertension, defined as new-onset blood pressure ≥140/90 mmHg after 20 weeks without proteinuria or other organ dysfunction, which usually resolves postpartum; preeclampsia, characterized by hypertension after 20 weeks accompanied by proteinuria or evidence of end-organ involvement such as thrombocytopenia or renal insufficiency; and eclampsia, a severe progression of preeclampsia marked by seizures.^[43] In severe cases of preeclampsia, HELLP syndrome may develop, involving hemolysis, elevated liver enzymes, and low platelet count, further complicating maternal and fetal outcomes.^[47] Key risk factors include primiparity (first pregnancy), maternal obesity (BMI ≥30 kg/m²), and a history of preeclampsia in previous pregnancies, which can increase recurrence risk by up to 20-40%.^[48]^[49] Other contributors encompass multiple gestation, advanced maternal age (>35 years), and pre-existing conditions like chronic hypertension or diabetes, though these must be differentiated from non-pregnancy secondary causes.^[50] Maternal risks from these disorders include stroke, placental abruption, and acute kidney injury, while fetal complications encompass intrauterine growth restriction, preterm birth, and stillbirth due to compromised uteroplacental perfusion.^[51]^[52] Delivery remains the definitive treatment, typically recommended after 37 weeks for gestational hypertension and earlier for preeclampsia to mitigate these risks.^[47]

Uncommon Causes

Pheochromocytoma

Pheochromocytoma is a rare neuroendocrine tumor arising from chromaffin cells in the adrenal medulla, accounting for approximately 0.1-0.6% of all hypertension cases and less than 1% of secondary hypertension cases, particularly in adults aged 30-50 years.^[53]^[54] These tumors secrete excessive catecholamines, such as epinephrine and norepinephrine, leading to paroxysmal or sustained hypertension through episodic vasoconstriction and increased cardiac output. Approximately 10% of pheochromocytomas are malignant, and another 10% occur extra-adrenally as paragangliomas, which share similar catecholamine-mediated effects but may present with additional symptoms related to tumor location.^[55] Unlike primary aldosteronism, which involves mineralocorticoid excess from the adrenal cortex, pheochromocytoma originates in the medulla and produces intermittent hypertensive crises rather than steady elevation.^[56] The pathophysiology involves autonomous release of catecholamines that bind to alpha- and beta-adrenergic receptors, causing acute surges in blood pressure often exceeding 180/110 mmHg during paroxysmal episodes. Sustained hypertension develops in about 50% of cases due to chronic catecholamine exposure, while the remaining patients experience intermittent spikes superimposed on normal or low baseline pressures. Between episodes, orthostatic hypotension may occur secondary to catecholamine-induced downregulation of alpha-2 receptors and relative hypovolemia from persistent vasoconstriction.^[57] This intermittency distinguishes pheochromocytoma from more consistent causes of secondary hypertension, such as renal parenchymal disease.^[58] Clinically, pheochromocytoma presents with the classic triad of severe headache, palpitations, and diaphoresis in up to 80% of symptomatic patients, often triggered by posture changes, stress, or medications. Hypertension is the hallmark, affecting over 90% of cases, with paroxysmal elevations more common in younger patients and sustained forms in older ones. Associated features include anxiety, tremor, and pallor during attacks, with rare progression to life-threatening complications like myocardial infarction or stroke if undiagnosed.^[58] Approximately 25-35% of cases are hereditary, linked to syndromes such as multiple endocrine neoplasia type 2 (MEN2) or von Hippel-Lindau (VHL) disease, warranting genetic screening in all patients regardless of family history.^[56] Diagnosis relies on biochemical confirmation followed by imaging for localization. Elevated plasma-free metanephrines exhibit a sensitivity of 96% for detecting pheochromocytoma, making it the preferred initial test over urinary metabolites or catecholamines. Positive results prompt cross-sectional imaging with computed tomography (CT) or magnetic resonance imaging (MRI) of the abdomen and pelvis, which identify adrenal masses in over 90% of cases, with functional scans like MIBG scintigraphy used for extra-adrenal or metastatic disease.^[59]^[60]

Cushing syndrome

Cushing syndrome, characterized by chronic glucocorticoid excess, is a rare but important cause of secondary hypertension, primarily through cortisol-mediated effects on mineralocorticoid receptors and sympathetic activation. It accounts for approximately 0.5-1% of cases of secondary hypertension, with iatrogenic forms due to prolonged exogenous glucocorticoid use being more common than endogenous causes in clinical practice.^[2]^[61] The etiologies of Cushing syndrome include pituitary adenomas causing Cushing disease in about 70% of endogenous cases, adrenal tumors in 20%, and ectopic ACTH production in 10%. Iatrogenic Cushing syndrome arises from supraphysiologic doses of exogenous glucocorticoids, such as prednisone or dexamethasone, often administered for autoimmune or inflammatory conditions, and represents the majority of all Cushing syndrome cases overall.^[62]^[63] In terms of pathophysiology, excess cortisol binds to and activates mineralocorticoid receptors in the kidney, promoting sodium and water retention, volume expansion, and subsequent hypertension. Additionally, cortisol contributes to insulin resistance, endothelial dysfunction, and vascular remodeling, further exacerbating blood pressure elevation through increased sympathetic nervous system activity and reduced nitric oxide bioavailability. These mechanisms distinguish Cushing syndrome hypertension from other endocrine causes, as it involves glucocorticoid spillover rather than isolated mineralocorticoid excess.^[64]^[65] Clinically, patients with Cushing syndrome often present with characteristic features including central obesity, moon facies, violaceous abdominal striae, and proximal muscle weakness. Hypertension is observed in about 80% of cases, typically mild to moderate with systolic pressures around 140-160 mmHg, and it may lack the nocturnal dipping pattern due to disrupted cortisol circadian rhythm. These signs, particularly in younger adults with resistant hypertension, should prompt evaluation for glucocorticoid excess.^[65]^[66] Diagnosis begins with screening for hypercortisolism using a 24-hour urinary free cortisol measurement, where levels exceeding four times the upper limit of normal strongly suggest Cushing syndrome. Confirmation often involves the low-dose dexamethasone suppression test, in which failure of cortisol to suppress below 1.8 μg/dL after 1 mg dexamethasone administration indicates autonomous cortisol production. Further localization with ACTH levels and imaging follows positive screening.^[67]^[68]

Coarctation of the aorta

Coarctation of the aorta is a congenital narrowing of the descending thoracic aorta, typically just distal to the left subclavian artery, that serves as a vascular cause of secondary hypertension by obstructing blood flow and creating a pressure gradient across the narrowing. This condition accounts for approximately 0.2% of cases of secondary hypertension in adults and is often diagnosed in adolescence or young adulthood if not detected in infancy.^[69] The obstruction leads to hypertension confined primarily to the upper body, distinguishing it from more generalized forms of hypertension, and shares pathophysiological parallels with renovascular hypertension through activation of the renin-angiotensin-aldosterone system (RAAS). In terms of pathophysiology, the post-ductal narrowing increases blood pressure proximal to the coarctation to maintain upper body perfusion, while causing hypoperfusion in the lower limbs and activating the RAAS due to reduced renal blood flow. This results in elevated systemic renin levels and aldosterone secretion, perpetuating hypertension even after partial collateral vessel development. The mechanical obstruction also imposes a chronic afterload on the left ventricle, contributing to structural cardiac changes over time.^[70]^[71] Clinically, patients often present with a systolic blood pressure gradient exceeding 20 mmHg between the upper and lower extremities, diminished or delayed femoral pulses, and signs of collateral circulation such as rib notching visible on chest X-ray due to enlarged intercostal arteries. Coarctation is frequently associated with a bicuspid aortic valve in 45% to 75% of cases, which may contribute to additional aortic complications. Other features include upper extremity hypertension, headaches, and leg claudication during exercise.^[72]^[13]^[73] Complications of untreated coarctation include left ventricular hypertrophy from sustained upper body hypertension and the formation of aortic aneurysms due to turbulent flow and vessel wall stress. Historically, approximately 85% of patients with unrepaired coarctation survive into adulthood, though long-term risks include heart failure, aortic rupture, and reduced life expectancy.^[74]^[75] Diagnosis is confirmed through imaging, with echocardiography or magnetic resonance imaging (MRI) demonstrating a reduction in aortic diameter greater than 50% at the site of coarctation, along with a measurable pressure gradient. These modalities provide detailed visualization of the narrowing and associated anomalies, such as bicuspid aortic valve, without the need for invasive procedures in initial assessment.^[76]^[77]

Thyroid disorders

Thyroid disorders contribute to secondary hypertension in approximately 1-2% of cases, primarily through hyperthyroidism and hypothyroidism, with hyperthyroidism more frequently associated with systolic blood pressure elevation.^[78] These conditions arise from imbalances in thyroid hormone levels, which exert significant influence on cardiovascular hemodynamics, and are considered rare endocrine causes compared to more common etiologies like primary aldosteronism.^[2] In hyperthyroidism, excess thyroid hormones lead to increased cardiac output, heightened heart rate, and reduced systemic vascular resistance, resulting in predominantly systolic hypertension; additionally, enhanced sensitivity to catecholamines amplifies sympathetic nervous system activity, further elevating blood pressure.^[79] Conversely, hypothyroidism induces diastolic hypertension through increased peripheral vascular resistance, diminished cardiac output, reduced arterial compliance, and accelerated atherosclerosis, often compounded by hyperlipidemia that promotes vascular stiffness.^[80] Both forms typically manifest as mild hypertension, though the underlying mechanisms remain incompletely understood, involving interactions with endothelial function and the renin-angiotensin-aldosterone system.^[81] Clinical features of hyperthyroidism-related hypertension include tachycardia, weight loss, tremors, and widened pulse pressure, reflecting the hypermetabolic state and cardiovascular strain.^[82] In hypothyroidism, associated signs encompass bradycardia, fatigue, and elevated lipid levels, contributing to long-term vascular damage and diastolic pressure rise.^[83] Notably, hypertension in both conditions is often reversible upon thyroid hormone normalization through appropriate treatment, underscoring the importance of early detection.^[84] The most common causes are autoimmune: Graves' disease for hyperthyroidism, characterized by thyroid-stimulating immunoglobulins that drive hormone overproduction and systolic hypertension, and Hashimoto's thyroiditis for hypothyroidism, involving lymphocytic infiltration leading to glandular destruction and diastolic elevation.^[82] These disorders are rare in children, with incidence rates below 1% in pediatric populations, differing from more prevalent congenital or renal causes of secondary hypertension in youth.^[85] Diagnosis relies on thyroid function tests, with overt hyperthyroidism indicated by suppressed thyroid-stimulating hormone (TSH) levels below 0.1 mU/L and elevated free thyroxine (T4) or triiodothyronine (T3), while overt hypothyroidism features TSH above 10 mU/L with low free T4; subclinical variants may show milder TSH deviations with normal T4/T3, confirmed via repeat testing and clinical correlation.^[86]

Other rare causes

Primary hyperparathyroidism is a rare endocrine cause of secondary hypertension, accounting for approximately 1% of cases among identifiable etiologies. In this condition, excessive parathyroid hormone secretion leads to hypercalcemia, which promotes vasoconstriction and activates the renin-angiotensin-aldosterone system (RAAS), thereby elevating blood pressure.^[87]^[88] Patients often present with associated symptoms such as kidney stones, bone pain, and fatigue, alongside hypertension that may resolve following parathyroidectomy.^[87] Acromegaly, resulting from growth hormone excess, represents another uncommon contributor to secondary hypertension, with prevalence estimates below 1% in hypertensive populations. The pathophysiology involves insulin resistance, hyperinsulinemia-induced sodium retention, and direct vascular effects of growth hormone, leading to increased cardiac output and peripheral resistance. Clinical manifestations typically include coarsened facial features, enlarged extremities, and hypertension resistant to standard therapy until the underlying pituitary adenoma is addressed.^[89]^[90] Chronic exposure to environmental toxins like lead and arsenic can induce secondary hypertension through renal toxicity, collectively comprising less than 0.5% of cases. Lead accumulates in the kidneys, causing tubulointerstitial damage, impaired sodium excretion, and subsequent hypertension, often in occupational settings such as battery manufacturing or mining. Arsenic exposure, commonly via contaminated drinking water, promotes endothelial dysfunction and oxidative stress, resulting in elevated blood pressure; higher cumulative doses correlate with increased hypertension risk. Symptoms may include a history of prolonged environmental or occupational contact, with nonspecific signs like fatigue or peripheral neuropathy.^[91]^[92] Erythropoietin abuse, particularly among athletes seeking performance enhancement, elevates blood pressure by increasing red blood cell mass and blood viscosity, which heightens vascular resistance; this mechanism mirrors therapeutic erythropoietin use but occurs in non-renal failure contexts and affects a negligible fraction of secondary hypertension cases. Scleroderma renal crisis, a complication of systemic sclerosis, causes acute severe hypertension through renovascular vasospasm and endothelial injury, leading to rapid renal failure; it occurs in about 10% of diffuse systemic sclerosis patients but is exceedingly rare as an isolated hypertension etiology.^[93]^[94] These miscellaneous rare causes together represent under 1% of secondary hypertension instances and warrant consideration in patients with atypical features, such as refractory hypertension or suggestive exposure histories, to guide targeted evaluation.^[2]

Diagnosis

Clinical history and physical examination

The clinical history plays a pivotal role in identifying potential secondary hypertension, as certain features distinguish it from essential hypertension. Key elements include the age of onset, with hypertension developing before age 30 or after age 55 raising suspicion, particularly in non-obese individuals without a family history of high blood pressure.^[1]^[2] A family history of endocrine disorders, such as early-onset hypertension or stroke before age 40, may suggest conditions like primary aldosteronism.^[95] Patients should be queried about symptoms of obstructive sleep apnea (OSA), including loud snoring, witnessed apneas, and daytime somnolence, as OSA is a common reversible cause.^[2] A thorough medication review is essential to identify inducing agents, such as nonsteroidal anti-inflammatory drugs, corticosteroids, oral contraceptives, or recreational substances like cocaine and alcohol.^[95]^[2] In women of childbearing age, pregnancy status must be assessed due to risks like preeclampsia.^[2] Exposure to environmental toxins, such as lead or excessive alcohol, should also be explored.^[2] Red flags in the history that warrant further evaluation for secondary causes include resistant hypertension, defined as blood pressure above goal despite adherence to three or more antihypertensive medications at optimal doses, including a diuretic, or requiring four or more medications to achieve control.^[10] The 2025 American Heart Association (AHA) guidelines emphasize screening all adults with hypertension for resistant hypertension to identify opportunities for addressing secondary etiologies, such as primary aldosteronism.^[10] Other indicators are labile blood pressure fluctuations, symptoms of hypokalemia (e.g., muscle weakness or cramps), and episodic symptoms like severe headaches, palpitations, or sweating, which may point to pheochromocytoma.^[2]^[95] A targeted history can identify a significant proportion of secondary hypertension cases, guiding subsequent diagnostic steps.^[54] The physical examination complements the history by revealing observable signs suggestive of underlying causes. Blood pressure should be measured in both arms and legs to detect discrepancies indicative of coarctation of the aorta.^[54]^[2] Fundoscopic examination is performed to assess for hypertensive retinopathy, which may reflect severe or accelerated hypertension.^[2] Auscultation for an abdominal bruit, particularly systolic-diastolic, suggests renovascular disease.^[54]^[2] Palpation and auscultation of pulses can identify radio-femoral delay or diminished femoral pulses in coarctation.^[54] For Cushing syndrome, inspection may reveal moon facies, central obesity, or violaceous striae.^[95]^[2] In evaluating for OSA, measurement of neck circumference greater than 40 cm in men or 36 cm in women is a key physical clue, as it correlates with increased risk.^[20] Overall, the physical exam is crucial for detecting clues like these, enhancing suspicion for secondary hypertension when combined with history.^[54]

Laboratory tests

Laboratory testing plays a crucial role in evaluating secondary hypertension by providing objective biomarkers that help identify underlying renal, endocrine, and other causes, often prompted by clues from clinical history and physical examination.^[54] Routine laboratory evaluations typically include a complete blood count (CBC) to assess for anemia or polycythemia that may suggest renal or endocrine disorders, serum electrolytes to detect hypokalemia indicative of hyperaldosteronism, blood urea nitrogen (BUN) and creatinine to evaluate renal function, and urinalysis to identify proteinuria or hematuria suggestive of renal parenchymal disease.^[10] Estimated glomerular filtration rate (eGFR) is calculated from serum creatinine to stage chronic kidney disease, which accounts for a significant portion of secondary hypertension cases.^[2] Targeted hormone assays are essential for screening endocrine etiologies. The plasma renin-aldosterone ratio (ARR) is a key initial test for primary aldosteronism, with the 2025 Endocrine Society guideline recommending screening all patients with hypertension using morning serum aldosterone and plasma renin levels, alongside potassium measurement.^[39] A positive screen is indicated by suppressed renin (plasma renin activity ≤1 ng/mL/h or direct renin concentration ≤8.2 mU/L) and aldosterone ≥10 ng/dL by immunoassay.^[39] For pheochromocytoma, plasma free metanephrines or 24-hour urinary fractionated metanephrines are recommended as first-line tests due to their high sensitivity.^[54] Thyroid function is assessed with thyroid-stimulating hormone (TSH) to detect hypo- or hyperthyroidism, while Cushing syndrome screening involves 24-hour urinary free cortisol or late-night salivary cortisol.^[2] Plasma catecholamines may be measured in select cases for pheochromocytoma confirmation.^[96] These laboratory tests are instrumental in identifying the majority of endocrine and renal causes of secondary hypertension, facilitating targeted further evaluation and management.^[97]

Imaging and specialized investigations

Imaging and specialized investigations in secondary hypertension are employed to identify and confirm structural or functional abnormalities underlying the condition, guided by clinical suspicion and prior laboratory findings such as electrolyte imbalances or hormone elevations. These modalities are recommended selectively to avoid unnecessary radiation exposure and costs, particularly in low-risk patients without suggestive features like resistant hypertension or abrupt onset. According to the 2025 AHA/ACC Guideline, routine imaging is not advised in low-risk cases but is indicated when laboratory tests raise suspicion for specific etiologies, such as renovascular disease or endocrine disorders.^[4] Similarly, the 2023 ESH Guidelines emphasize targeted use based on biochemical screening to localize abnormalities efficiently.^[98] For suspected renovascular hypertension, renal imaging begins with non-invasive duplex ultrasound, which measures peak systolic velocities to detect renal artery stenosis, offering high sensitivity (around 90%) for hemodynamically significant lesions greater than 60%. If ultrasound is inconclusive or contraindicated, computed tomography (CT) or magnetic resonance (MR) angiography provides detailed visualization of arterial narrowing due to atherosclerosis or fibromuscular dysplasia, with MR angiography preferred in patients with renal impairment to avoid iodinated contrast. Renal scintigraphy with agents like technetium-99m-MAG3 can further assess functional significance by evaluating differential renal perfusion and function, particularly in bilateral disease. These approaches are prioritized in cases with laboratory evidence of asymmetric kidney function or renin elevation.^[4]^[98] Adrenal imaging is indicated following biochemical confirmation of hyperaldosteronism or catecholamine excess. CT or MRI of the adrenal glands identifies adenomas or hyperplasia, with CT demonstrating high resolution for lesions as small as 5 mm and MRI useful for characterizing pheochromocytomas due to their hyperintense T2 signal. For primary aldosteronism, adrenal vein sampling is a specialized invasive procedure to lateralize aldosterone overproduction, achieving over 95% accuracy when performed by experienced operators, thus guiding potential surgical intervention. In pheochromocytoma, meta-iodobenzylguanidine (MIBG) scintigraphy evaluates for metastatic disease or extra-adrenal involvement, with sensitivity exceeding 85% for functional tumors.^[4]^[98] Vascular imaging targets congenital or acquired anomalies like coarctation of the aorta. Echocardiography quantifies the transcoarctation pressure gradient via Doppler, with gradients over 20 mmHg suggesting significant obstruction, and is often the initial modality due to its non-invasive nature and ability to assess associated cardiac effects. Chest X-ray may reveal rib notching from collateral circulation in chronic coarctation, providing a simple screening clue. CT or MR angiography confirms the diagnosis and extent of narrowing, essential for preoperative planning.^[4]^[98] Specialized investigations extend to functional assessments for conditions like obstructive sleep apnea (OSA), where polysomnography measures the apnea-hypopnea index (AHI), with values above 15 events per hour confirming diagnosis and a prevalence of 70-80% in individuals with resistant hypertension.^[99] This test is recommended when symptoms or laboratory hints like insulin resistance suggest OSA. Overall, these investigations enhance diagnostic precision when integrated with clinical and lab data, per both major guidelines.^[4]^[98]

Management

General principles

The management of secondary hypertension prioritizes the identification and targeted treatment of the underlying etiology, which can lead to cure or significant improvement in blood pressure control, alongside universal lifestyle modifications such as the DASH diet, regular aerobic exercise, weight loss, and sodium restriction to <2,300 mg/day.^[10]^[2] These nonpharmacologic interventions are recommended for all patients, regardless of the specific cause, to enhance overall cardiovascular health and support pharmacotherapy adherence.^[98] Multidisciplinary care involving specialists like endocrinologists for endocrine-related causes or nephrologists for renal issues is essential to coordinate etiology-specific interventions with blood pressure management.^[2] Blood pressure targets for most adults with secondary hypertension align with general hypertension guidelines, aiming for <130/80 mm Hg to reduce cardiovascular risk, with monitoring post-treatment to assess reversibility of hypertension after addressing the underlying cause.^[10] These targets may be adjusted based on comorbidities, such as chronic kidney disease, but should be achieved through a combination of lifestyle changes and pharmacotherapy tailored to the etiology—for instance, avoiding ACE inhibitors or ARBs in cases of bilateral renovascular disease to prevent acute kidney injury.^[2] Initial pharmacotherapy should incorporate cause-appropriate agents, such as mineralocorticoid receptor antagonists for primary aldosteronism, with escalation to multidrug regimens if monotherapy is insufficient.^[10]^[98] Ongoing monitoring includes home blood pressure tracking to confirm control and detect white-coat or masked effects, along with annual laboratory assessments of electrolytes, renal function, and other relevant parameters to evaluate treatment efficacy and side effects.^[10] To prevent complications, cardiovascular risk reduction strategies such as statin therapy are indicated if patients meet criteria for dyslipidemia or elevated atherosclerotic cardiovascular disease risk, integrated into the broader management plan.^[2]

Cause-specific treatments

Treatment of secondary hypertension requires addressing the underlying etiology to achieve optimal blood pressure control and potentially reverse the hypertensive state. For obstructive sleep apnea (OSA), continuous positive airway pressure (CPAP) therapy is the cornerstone intervention, modestly reducing systolic blood pressure by 2 to 4 mmHg on average, with greater benefits observed in patients with uncontrolled hypertension at baseline.^[100] Weight loss through lifestyle modifications or bariatric interventions further supports blood pressure reduction in OSA-associated hypertension by alleviating airway obstruction and improving metabolic factors.^[101] In renal parenchymal disease, renin-angiotensin-aldosterone system (RAAS) blockers such as angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) are recommended as first-line therapy to mitigate proteinuria and slow progression to end-stage renal disease, though close monitoring for hyperkalemia is essential due to impaired renal excretion.^[102] For patients progressing to end-stage renal disease, dialysis effectively manages volume overload and uremia, often leading to improved blood pressure control.^[2] Renovascular hypertension due to fibromuscular dysplasia is primarily managed with percutaneous transluminal angioplasty, which offers high technical success rates and durable blood pressure improvement without routine stenting, as balloon angioplasty alone suffices in most cases.^[28] In contrast, atherosclerotic renovascular disease typically responds better to medical optimization with RAAS inhibitors or other antihypertensives, reserving revascularization for cases with progressive renal decline or refractory hypertension.^[103] Primary aldosteronism treatment hinges on subtype: mineralocorticoid receptor antagonists like spironolactone or eplerenone provide effective medical control of hyperaldosteronism and hypertension in bilateral cases, with the 2025 Endocrine Society guidelines emphasizing early initiation of these agents over epithelial sodium channel inhibitors for broader biochemical and cardiovascular benefits.^[104] For unilateral disease confirmed by adrenal vein sampling, laparoscopic adrenalectomy cures hypertension in 30% to 60% of patients, normalizing aldosterone excess and often reducing or eliminating the need for antihypertensive medications.^[105] Drug-induced secondary hypertension is managed by promptly discontinuing the offending agent, such as nonsteroidal anti-inflammatory drugs or cyclosporine, which typically resolves the elevation within days to weeks.^[106] Alternatives should be selected based on the indication, for example, substituting estrogen-containing contraceptives with progestin-only options to avoid estrogen-mediated sodium retention.^[2] In pregnancy-associated hypertension, including gestational hypertension and preeclampsia, first-line antihypertensives include labetalol or extended-release nifedipine, which safely lower blood pressure without compromising uteroplacental perfusion, targeting a systolic range of 120 to 160 mmHg.^[107] For severe preeclampsia, prompt delivery remains the definitive treatment, particularly after 34 weeks' gestation, to avert maternal and fetal complications.^[108] Among less common causes, pheochromocytoma-induced hypertension necessitates preoperative alpha-blockade with nonselective agents like phenoxybenzamine to stabilize hemodynamics and prevent intraoperative crises during tumor resection.^[109] For Cushing syndrome, ketoconazole inhibits adrenal steroidogenesis, improving hypertension and hypokalemia in 40% to 50% of patients as a bridge to surgery or in inoperable cases.^[110] Surgical repair of coarctation of the aorta, via resection and end-to-end anastomosis or patch aortoplasty, normalizes upper extremity blood pressure in approximately 70% of patients postoperatively, though lifelong surveillance for recoarctation is required.^[111] Thyroid disorders contributing to hypertension, such as hyperthyroidism, are addressed by restoring euthyroid status with antithyroid drugs or definitive therapy, which concurrently ameliorates blood pressure elevations.^[2]

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KDIGO 2021 Clinical Practice Guideline for the Management of ...
Recommendation 4.1: We recommend that a dihydropyridine calcium channel blocker (CCB) or an ARB be used as the first-line antihypertensive agent in adult kidney ...
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Renovascular Hypertension Treatment & Management
Nov 16, 2024 · Renovascular hypertension (RVHT) reflects ... Factors that should prompt evaluation for renal artery disease include the following :.
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Primary Aldosteronism: An Endocrine Society Clinical Practice ...
Jul 14, 2025 · The Guideline Development Panel outlined both minimal-withdrawal and no-withdrawal strategies of interfering medications before screening ( ...
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Clinical Management of Primary Aldosteronism: An Update
Jul 24, 2024 · Primary aldosteronism (PA) implies excess cardiovascular damage and events and is a common curable cause of hypertension. · A wide range of ...
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Drug-Induced Hypertension - U.S. Pharmacist
Sep 18, 2008 · Drug-induced blood pressure elevations represent an important and modifiable cause of secondary hypertension; therefore, it is imperative that ...
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Hypertension in Pregnancy and Postpartum: Current Standards and ...
Feb 17, 2025 · Any evidence of hypertension before 20 weeks of gestation is classified as chronic hypertension, and new-onset hypertension after that time is ...
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Hypertension and Pregnancy Treatment & Management
Apr 25, 2025 · Intravenous (IV) labetalol, IV hydralazine, and oral immediate-release nifedipine are the most common agents recommended.
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Pheochromocytoma Medication - Medscape Reference
Apr 26, 2024 · Preoperative preparation requires combined alpha and beta blockade to control blood pressure and to prevent an intraoperative hypertensive crisis.
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Ketoconazole in Cushing's Disease: Is It Worth a Try?
Forty patients (20%) received ketoconazole as a presurgical treatment; 40% to 50% of these patients showed improvement of hypertension, hypokalemia, and ...Patients and Methods · Results · Discussion
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Heart team approach for comprehensive management of aortic ...
Jan 24, 2022 · Open repair has outstanding early postoperative morbidity and mortality (<1%) and early resolution of hypertension in 13–76% of patients. This ...Missing: normalization | Show results with:normalization