Epidemiology, risk factors, and etiology of hypertension in children and adolescents

INTRODUCTION — Hypertension (HTN) begins in childhood and adolescence and contributes to the early development of cardiovascular disease in adult life. The supporting data include clinical studies that demonstrate cardiovascular structural and functional changes in children with HTN and autopsy studies that have shown an association of blood pressure (BP) with atherosclerotic changes in the aorta and heart in children and young adults. In hypertensive adults, multiple randomized trials have shown that reduction of BP by antihypertensive therapy reduces cardiovascular morbidity and mortality. The magnitude of the benefit increases with the severity of the HTN. (See "Overview of hypertension in adults".)

Based on these observations, identifying and successfully treating HTN in children is likely to have an important impact on long-term outcomes of cardiovascular disease.

The epidemiology, risk factors, and etiology of childhood HTN will be reviewed here. Related content can be found in the following topic reviews:

●(See "Definition and diagnosis of hypertension in children and adolescents".)

●(See "Evaluation of hypertension in children and adolescents".)

●(See "Overview of risk factors for development of atherosclerosis and early cardiovascular disease in childhood", section on 'Hypertension'.)

●(See "Nonemergent treatment of hypertension in children and adolescents".)

●(See "Etiology, clinical features, and diagnosis of neonatal hypertension".)

DEFINITIONS

●Hypertension (HTN) – For children in the United States, the 2017 American Academy of Pediatrics (AAP) guidelines for screening and managing high blood pressure (BP) for children and adolescents definitions are used to categorize BP for two different age groups (table 1) [1]. BP percentiles are based on sex, age, and height (table 2 and table 3).

Further details, including definitions of HTN used outside of the United States, are discussed in a separate topic review. (See "Definition and diagnosis of hypertension in children and adolescents", section on 'Definitions'.)

Childhood HTN is divided into two categories, depending on whether or not an underlying cause can be identified (table 4):

•Primary HTN – No identifiable cause is found

•Secondary HTN – An underlying cause is identified

●Other categories – Other classifications of BP are based on ambulatory BP monitoring [2]:

•White coat hypertension – White coat or isolated office HTN is defined as office BP readings ≥95^th percentile but with normal values outside of the clinical setting. Studies suggest a prevalence as high as one-third to one-half of children being evaluated for persistently elevated, casual BP [3,4].

It is possible that white coat HTN in children represents two populations: one that is destined to develop primary HTN (prehypertensive) [5,6], and one that remains normotensive outside of the clinical setting. In adults, white coat HTN appears to be a prehypertensive condition with increased left ventricular mass and progression to sustained HTN. Limited data in children also suggest that some children with white coat HTN progress to ambulatory HTN. (See "Ambulatory blood pressure monitoring in children", section on 'White coat hypertension'.)

•Masked hypertension – Masked HTN is characterized by normal BP in clinic or office and a high ambulatory BP outside of the office, including home. Masked HTN is associated with obesity and increased left ventricular mass, which are risk factors for early adult cardiovascular disease [2]. (See "Ambulatory blood pressure monitoring in children", section on 'Masked hypertension'.)

Patient selection for ambulatory BP monitoring, interpretation of the results, and clinical implications of these diagnoses are discussed separately. (see "Ambulatory blood pressure monitoring in children", section on 'Classification of blood pressure')

EPIDEMIOLOGY

●Prevalence – In the United States, the prevalence of HTN in children and adolescents is approximately 4 percent, using criteria defined by the 2017 American Academy of Pediatrics (AAP) guideline [7,8]. A similar prevalence for pediatric HTN was noted by a systematic review and meta-analysis of studies conducted in many different countries and regions, including both rural and urban populations [9]. This study used a strict definition of HTN, based on blood pressure (BP) measurements conducted at least on three separate occasions in individuals up to 19 years of age. It did not use the definition from the 2017 AAP guidelines, which may have resulted in a higher prevalence.

●Impact of choice of definition – The risk of elevated BP and HTN depends on the definition used to categorize BP. Several studies reported higher rates of elevated BP and HTN when the BP definitions in the 2017 AAP guidelines were used compared with an earlier definition (Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents) or the 2016 European Society of Hypertension guidelines [7,10-16]. As a result, use of the 2017 AAP guidelines identifies more children with elevated BP and HTN who will require additional follow-up and possibly treatment. Of note, males and individuals who with overweight or obesity were more likely to be reclassified with a higher category of BP (ie, elevated BP or HTN) [7,10,12]. These findings were confirmed by a prospective study that reported that the prevalence of HTN was higher when using the 2017 guidelines compared with the previous guideline of the Fourth Report in a high-risk population of adolescents with obesity and type 2 diabetes (13 versus 8 percent, respectively) [17].

RISK FACTORS FOR PRIMARY HYPERTENSION — Risk factors for primary HTN can be separated into modifiable and nonmodifiable factors.

Modifiable risk factors

●Obesity – There are strong observational data linking the risk of HTN to excess body weight in school-aged children [18-23]. By contrast, a report from the Bogalusa Heart Study showed that mean systolic and diastolic blood pressure (BP) levels did not increase, despite a rise in the prevalence of obesity from 6 to 17 percent over the study period from 1974 to 1993 [24]. Nevertheless, within this cohort of 11,478 children, there was a positive correlation of body mass index (BMI) and BP levels. However, these results suggest that other factors may have ameliorated the expected increase in BP due to the increasing prevalence of obesity. (See "Definition, epidemiology, and etiology of obesity in children and adolescents" and "Overview of the health consequences of obesity in children and adolescents".)

The relationship between elevated BP and weight appears to begin in early childhood. In a retrospective review of primary care visits of 18,618 children between 2 and 19 years of age, systolic and diastolic BP increased with increasing BMI in all age groups, including children between two and five years of age [25]. In a longitudinal study, systolic BP and weight-for-length were measured in 530 children from birth to three years of age [26]. An increase in the weight-for-length in the first six months of life was associated with higher systolic BP at three years of life, particularly among infants who were thin at birth. In another longitudinal study, weight gain during infancy and early childhood was the predominant predictor of HTN at age five years, whereas current weight status was the predominant predictor at age 10 years [27].

The metabolic syndrome is a clustering of conditions that include obesity, high BP, insulin resistance, abnormal glucose tolerance, and abnormal lipid levels. The association of abnormal lipids with BP was shown in a retrospective, case-control study of 497 patients 2 to 18 years of age that found that significantly more boys with high BP had low high-density lipoprotein cholesterol compared with boys with normal BP (49.4 versus 27.6 percent, respectively) [28]. (See "Metabolic syndrome (insulin resistance syndrome or syndrome X)".)

●Dietary sodium intake – Observational data have shown that BP levels in children increase with higher sodium intake. In a population-based study in the United States, the risk for elevated systolic BP was higher in children with an elevated sodium intake (defined as >1.5 times reference daily intake) compared with those with a lower sodium intake (odds ratio [OR] 1.36, 95% CI 1.04-1.77) after controlling for both overall and central obesity [19]. In a meta-analysis of children with elevated BP, systolic BP increased by 6.3 mmHg (95% CI 2.9-9.6) and diastolic BP increased by 3.5 mmHg (95% CI 1.2-5.7) for every additional gram of sodium intake [29].

●Obstructive sleep apnea (OSA) – OSA, which causes intermittent partial or complete occlusion of the upper airway during sleep, is a risk factor for increased BP, independent of obesity [30,31]. (See "Cardiovascular consequences of obstructive sleep apnea in children", section on 'Changes in blood pressure'.)

One observational study reported that improvement in sleep-disordered breathing was associated with improved BP control [32]. Similarly, adenotonsillectomy for OSA in children modestly reduces BP [33,34].

●Physical activity – Studies of the relationship between physical activity during childhood and HTN risk reach mixed conclusions. A large meta-analysis found a modest beneficial effect of physical activity on BP and other cardiovascular risk factors [35]. A separate review concluded that regular physical activity reduces BP by approximately 2 mmHg [36]. Physical activity may also contribute to weight control. In a meta-analysis, aerobic exercise improved BP, body weight, and other components of the metabolic syndrome [37]. (See "Pediatric prevention of adult cardiovascular disease: Promoting a healthy lifestyle and identifying at-risk children", section on 'Physical activity'.)

●Breastfeeding (protective) – There are reports that breastfeeding is associated with lower BPs in childhood, as illustrated by two prospective cohort studies [38-40]. (See "Infant benefits of breastfeeding", section on 'Limited evidence for benefit'.)

•In the first study, 7276 infants were evaluated at 7.5 years of age [38]. Those who were breastfed as infants had systolic and diastolic BPs that were 1.2 mmHg and 0.9 mmHg lower than in infants who were never breastfed. The reduction in both systolic and diastolic pressures was greater in infants who were exclusively breastfed, and the systolic BP reduction increased with the duration of breastfeeding.

•Similar findings were found in 7223 singleton infants evaluated at five years of age [40]. Those who were breastfed for six months had systolic BP that was 1.2 mmHg lower than in infants who had been breastfed less than six months or not at all [40].

●Tobacco exposure – Both active and passive tobacco exposure appears to increase BP. This was illustrated by a multivariate analysis of data from the 2007 to 2016 National Health and Nutrition Examination Survey (NHANES) of 8520 children (mean age 13.1 years), which reported that children exposed to tobacco (either active or passive) were more likely to have elevated BP compared with those without tobacco exposure, after adjustment for potential confounders (OR 1.31, 95% CI 1.06-1.61) [41]. (See "Prevention of smoking and vaping initiation in children and adolescents" and "Secondhand smoke exposure: Effects in children", section on 'Cardiovascular disease'.)

●Childhood adversity – Adverse childhood experiences (ACEs) describe traumatic events of childhood, including abuse, neglect, parental mental health problems, and household dysfunction, and are associated with increased mortality and morbidity throughout the life course. Observational data have linked ACEs to increased risk of overweight and obesity, cardiovascular disease (coronary heart disease and stroke), and HTN [42-44]. A systematic review reported a consistent positive correlation between violence experienced during childhood and cardiovascular outcomes, including HTN [43]. Another study found that individuals with multiple ACE exposures had more rapid increases in systolic and diastolic BP after age 30 compared with those with fewer ACE exposures [44].

●Prenatal and neonatal factors – There is increasing evidence that prenatal and neonatal factors contribute to higher BP [45,46]. The possible role of low birth weight in the development of primary HTN is discussed in greater detail separately. (See "Possible role of low birth weight in the pathogenesis of primary (essential) hypertension".)

In addition, a systematic review reported that in utero exposure to preeclampsia was associated with an increase in systolic (mean 2.4 mmHg) and diastolic (mean 1.4 mmHg) BP, as well as an increase in BMI (mean 0.62 kg/m²) [47].

However, for children with chronic kidney disease, there appears to be no additional effect of an abnormal birth history on BP. This was illustrated in a report from the Chronic Kidney Disease in Children Study, which found no difference in BP or the rate of chronic kidney disease progression between patients with an abnormal birth history (birth weight <2500 g, gestational age <36 weeks, or small for gestational age) and those with a normal birth history [48].

Nonmodifiable risk factors

●Sex – In the United States and Canada, the prevalence of HTN and prehypertension is greater in boys than in girls [18,22]. In a Canadian cohort study of adolescents, boys were more likely to have high systolic BP (>90^th percentile) compared with girls in 7^th (OR 1.29, 95% CI 0.77-2.16), 9^th (OR 1.98, 95% CI 1.35-2.93), and 11^th grades (OR 2.74, 95% CI 1.52-4.94).

●Family history – A family history of HTN is present in as many as 70 to 80 percent of all patients with primary HTN (also referred to as essential HTN), which has no identifiable underlying etiology, and in approximately 50 percent of hypertensive children [49]. In particular, early-onset (age <45 years) and not late-onset parental HTN (≥65 years) is associated with HTN in offspring [50].

In patients with primary HTN, elevated BP is thought to result from the interaction of multiple genes and environmental factors. It has been estimated that genetic factors account for approximately 30 percent of the variation in BP in various populations [51,52] and as much as 60 to 70 percent of HTN in families [53]. (See "Genetic factors in the pathogenesis of hypertension".)

The best evidence for genetic factors influencing BP values comes from BP correlations within families:

•The BP correlation is stronger between parents and children than between spouses [54].

•There is no significant BP correlation between parents and adopted children [55,56].

•Most studies in twins have shown that BP correlation is stronger between identical (monozygotic) twins than between fraternal (dizygotic) twins or siblings [54,57]. However, the observation that the BP correlation is stronger among dizygotic twins than among other first-degree relatives indicates a nongenetic environmental effect [58].

In both animal and human studies, a number of different genes have been evaluated, but their role remains uncertain in the pathogenesis of primary HTN. (See "Genetic factors in the pathogenesis of hypertension".)

●Race and ethnicity – In the United States, data suggest that the prevalence of HTN is greater in Black and Hispanic children compared with White and Asian children [18,59-61].

•In a study using NHANES data, the prevalence of BP ≥95^th percentile (on a single occasion) was 4.6, 4.2, and 3.3 in Mexican American, Black, and White children, respectively, during the study period of 1999 to 2002 [18].

•In a school-based screening program in Houston, Texas from 2000 to 2015, the rates for HTN were 3.1, 2.7, 2.6, and 1.7 percent for Hispanic, Black, White, and Asian adolescents (age 10 to 19 years), respectively [61]. However, the highest rate of HTN was in White adolescents with obesity (7.4 percent).

•Of 2368 girls enrolled at the age of 9 or 10 years in the National Heart, Lung, and Blood Institute Growth and Health Study from 1986 to 1997, the overall incidence of HTN based on two clinic visits was greater in Black girls compared with White girls (5 versus 2.1 percent, respectively) when measured at annual visits through age 18 to 19 years [60]. The incidence increased to 10.5 and 3.8 percent in Black and White girls, respectively, whose BMIs were greater than the 95^th percentile, and was lower in those with normal BMI (<85^th percentile, 3.5 versus 1.7 percent).

Among adults in the United States, data from NHANES III showed that non-Hispanic Black Americans have a higher burden of HTN than other groups (figure 1A-B) [62]. Multiple factors that might contribute to this observed difference have been suggested. (See "The prevalence and control of hypertension in adults", section on 'Prevalence of hypertension' and "Burden of hypertension in Black individuals".)

ETIOLOGY — Causes of childhood HTN are separated into two classes (table 4):

●Primary HTN – No underlying cause is identified. This is a diagnosis of exclusion.

●Secondary HTN – An identifiable cause is determined (table 5). In children with secondary HTN, the underlying disorder may be curable with complete resolution of HTN.

Primary hypertension — As in adults, primary HTN is the most common cause for HTN in children and young adults in the United States, particularly in those older than six years with a positive family history and excessive body weight [1,63]. It is also more common in African American children.

The incidence of primary versus secondary HTN varies between countries and populations, likely due to differences in risk factors, referral patterns, and/or evaluation processes. (See 'Risk factors for primary hypertension' above.)

Secondary hypertension — There are a number of causes of secondary HTN (table 5). Specific symptoms (table 6) and findings (table 7) may point to a particular disorder.

The prevalence of secondary versus primary HTN and the causes of secondary HTN vary, depending on the country, age of the cohort, and risk factors [64-67]. Examples of the range of diagnoses made in referral centers are:

●In a 1992 review of children with sustained HTN from Poland, 351 of 636 children (55 percent) had a known secondary cause [64]. The most common were kidney disease (68 percent) and endocrine and renovascular diseases (11 and 10 percent, respectively). Almost all children (98 percent) younger than 15 years of age had a secondary cause, whereas 75 percent of adolescents had primary HTN.

●In an observational series of children with sustained HTN from the United States, 102 of 132 (77 percent) had an identified secondary cause [65]. The most common cause was kidney parenchymal or renovascular disease (67 percent), mostly glomerulonephritis (GN) or reflux nephropathy. Ten percent had secondary causes other than kidney disease.

The following sections outline different etiologies of chronic (ie, persistent) secondary HTN.

Kidney disease

●Kidney parenchymal disease – A variety of intrinsic kidney disorders is associated with HTN and includes the following:

•GN – HTN is a manifestation of acute and chronic glomerular disorders. In children, the most common form of acute glomerular disease is poststreptococcal GN, which follows after a streptococcal infection. Immunoglobulin A (IgA) vasculitis (ie, Henoch-Schönlein purpura) can present with kidney manifestations, including HTN. In children, chronic glomerular disorders associated with elevated blood pressure (BP) include IgA nephropathy, membranoproliferative GN, or lupus nephritis. (See "Poststreptococcal glomerulonephritis" and "IgA nephropathy: Clinical features and diagnosis" and "Lupus nephritis: Diagnosis and classification" and "Membranoproliferative glomerulonephritis: Classification, clinical features, and diagnosis" and "IgA vasculitis (Henoch-Schönlein purpura): Clinical manifestations and diagnosis".)

In children with GN, the most common mechanisms of HTN are volume expansion due to salt and water retention (as in acute poststreptococcal GN) and activation of the renin-angiotensin system. Other common presenting features of glomerular disorders include hematuria, oliguria, peripheral edema, and elevated serum creatinine or blood urea nitrogen. (See "Overview of hypertension in acute and chronic kidney disease".)

•Parenchymal scarring – Kidney parenchymal scarring can be a sequelae of acute pyelonephritis and may be associated with vesicoureteral reflux. It is also seen in children with congenital anomalies of the kidney and urinary tract. (See "Clinical presentation, diagnosis, and course of primary vesicoureteral reflux" and "Treatment and prognosis of Shiga toxin-producing Escherichia coli (STEC) hemolytic uremic syndrome in children", section on 'Hypertension' and "Urinary tract infections in infants older than one month and children less than two years: Acute management, imaging, and prognosis", section on 'Prognosis'.)

•Chronic kidney disease – Chronic kidney disease of any cause can be associated with HTN because of volume expansion and other factors. In addition, children who have undergone kidney transplantation are at increased risk for HTN due to several different mechanisms, including rejection or the administration of drugs that increase BP. (See "Kidney transplantation in children: Complications", section on 'Hypertension' and 'Drugs and toxins' below and "Chronic kidney disease in children: Complications", section on 'Hypertension'.)

●Monogenic disorders – Many monogenic causes of HTN have been identified, many of which are due to gain-of-function mutations leading to salt and water retention or an increased mineralocorticoid activity. Some of the better-known forms are:

•Liddle syndrome (MIM #177200), due to a gain-of-function mutation in the sodium channel gene, is associated with HTN, low plasma renin and aldosterone levels, and hypokalemia. (See "Genetic disorders of the collecting tubule sodium channel: Liddle syndrome and pseudohypoaldosteronism type 1", section on 'Liddle syndrome'.)

•Pseudohypoaldosteronism type 2 (MIM #145260), also known as Gordon syndrome, is due to mutations in WNK kinases 1 and 4, which result in increased chloride reabsorption with sodium. It is characterized by HTN, hyperkalemia, normal kidney function, and low or low-normal plasma renin activity and aldosterone. (See "Etiology, diagnosis, and treatment of hypoaldosteronism (type 4 RTA)", section on 'Pseudohypoaldosteronism type 2 (Gordon's syndrome)'.)

•Familial hyperaldosteronism type 1 (MIM #103900), also known as glucocorticoid-remediable aldosteronism, is a disorder in which there is a chimeric gene formed from portions of the 11-beta-hydroxylase gene and the aldosterone synthase gene, which results in adrenocorticotropic hormone, stimulating aldosterone synthesis. (See "Familial hyperaldosteronism".)

•Congenital adrenal hyperplasia due to 11-beta-hydroxylase deficiency (MIM #202010) is a disorder that has been associated with multiple mutations of the CYP11B1 gene. (See "Uncommon congenital adrenal hyperplasias", section on '11-beta-hydroxylase deficiency'.)

•Apparent mineralocorticoid excess (MIM #218030) arises from mutations in HSD11B2, the gene encoding the enzyme 11-beta-hydroxysteroid dehydrogenase. The defective enzyme allows normal circulating concentrations of cortisol (which are much higher than those of aldosterone) to activate the kidney mineralocorticoid receptors, resulting in increased sodium absorption. (See "Apparent mineralocorticoid excess syndromes (including chronic licorice ingestion)".)

●Renovascular disease – HTN due to renovascular disease is due to a decrease in renal blood flow, resulting in increased plasma levels of renin, angiotensin, and aldosterone. Children with renovascular disease generally have stage 2 HTN [68]. (See 'Definitions' above.)

Causes of renovascular disease in children include:

•Fibromuscular dysplasia – Fibromuscular dysplasia is the most common etiology of renovascular disease [69,70]. It is characterized by arterial stenosis due to a noninflammatory, nonatherosclerotic process. Most children with fibromuscular dysplasia have stenosis tortuosity of visceral arteries, including abdominal aorta along with renal artery involvement [71]. (See "Clinical manifestations and diagnosis of fibromuscular dysplasia".)

•Umbilical arterial catheterization – During the newborn period, catheterization of the umbilical artery may lead to a clot in the renal artery, resulting in renal arterial injury and stenosis.

•Other – Other causes of renovascular disease include neurofibromatosis, arteritis, renal artery hypoplasia, and midaortic syndrome (segmental narrowing of the proximal abdominal aorta) [69,70,72]. (See "Neurofibromatosis type 1 (NF1): Pathogenesis, clinical features, and diagnosis" and "Clinical features and diagnosis of Takayasu arteritis" and "Clinical manifestations and diagnosis of polyarteritis nodosa in adults".)

Endocrinologic disease — Endocrinologic conditions associated with HTN include the following:

●Catecholamine excess – Catecholamine excess that results in HTN occurs in patients with pheochromocytoma and neuroblastoma and in those who use sympathomimetic drugs, including phenylpropanolamine (over-the-counter decongestant), cocaine, amphetamines, phencyclidine, epinephrine, phenylephrine, and terbutaline, and the combination of a monoamine oxidase inhibitor plus ingestion of tyramine-containing foods. (See "Pheochromocytoma and paraganglioma in children" and "Clinical presentation, diagnosis, and staging evaluation of neuroblastoma".)

●Corticosteroid excess – Corticosteroid excess is more commonly due to exogenous administration of glucocorticoids and rarely due to endogenous production of either glucocorticoids or mineralocorticoids. In both settings, corticosteroid excess results in HTN.

•Corticosteroid excess may be seen in patients with Cushing syndrome due to hypersecretion of adrenocorticotropic hormone. (See "Causes and pathophysiology of Cushing syndrome".)

•Mineralocorticoid excess that results in HTN may be seen in patients with congenital adrenal hyperplasia. Other rare causes of HTN due to mineralocorticoid excess include aldosterone-secreting tumors and the monogenic disorder of glucocorticoid-remediable aldosteronism. (See "Causes of primary adrenal insufficiency in children", section on 'Congenital adrenal hyperplasia' and "Familial hyperaldosteronism".)

●Other endocrinologic disorders – Other endocrinologic abnormalities associated with HTN include thyroid disorders (hypothyroidism and hyperthyroidism) and hypercalcemia (eg, hyperparathyroidism). (See "Clinical manifestations of hypothyroidism", section on 'Cardiovascular system' and "Cardiovascular effects of hyperthyroidism" and "Clinical manifestations of hypercalcemia", section on 'Cardiovascular'.)

Cardiac disease — Coarctation of the aorta is a well-known cause of HTN. The classic findings are HTN in the upper extremities, diminished or delayed femoral pulses, and low or unobtainable arterial BP in the lower extremities. The diagnosis is confirmed by echocardiogram. (See "Clinical manifestations and diagnosis of coarctation of the aorta".)

Drugs and toxins — A variety of drugs and toxins can cause chronic HTN, including the following:

●Glucocorticoids (see "Major adverse effects of systemic glucocorticoids", section on 'Cardiovascular effects')

●Oral contraceptives (see "Contraception: Hormonal contraception and blood pressure")

●Arsenic (see "Arsenic exposure and chronic poisoning", section on 'Cardiovascular')

●Cyclosporine and tacrolimus (see "Pharmacology of cyclosporine and tacrolimus", section on 'Hypertension')

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Hypertension in children".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●The Basics (see "Patient education: High blood pressure in children (The Basics)")

●Beyond the Basics topics (see "Patient education: High blood pressure in children (Beyond the Basics)" and "Patient education: High blood pressure treatment in children (Beyond the Basics)")

SUMMARY

●Clinical significance ‒ Hypertension (HTN) in childhood and adolescence contributes to premature atherosclerosis and the early development of cardiovascular disease. (See 'Introduction' above and "Overview of risk factors for development of atherosclerosis and early cardiovascular disease in childhood", section on 'Hypertension'.)

●Modifiable risk factors ‒ Modifiable risk factors include high sodium intake, overweight or obesity, lack of breastfeeding as an infant, exposure (active or passive) to tobacco smoke, and adverse childhood events (ACEs). In addition, white coat and masked HTN appear to increase the risk of primary HTN. (See 'Modifiable risk factors' above.)

●Nonmodifiable risk factors ‒ Nonmodifiable risk factors include male sex, Black and Hispanic race, and having a positive family history for HTN. (See 'Nonmodifiable risk factors' above.)

●Etiology ‒ The etiology of pediatric chronic HTN is divided into two categories (see 'Etiology' above):

•Primary HTN, in which no underlying cause is identified.

A family history of HTN is present in as many as 70 to 80 percent of all patients with primary HTN. In patients with primary HTN, elevated blood pressure (BP) is thought to result from the interaction of multiple genes and environmental factors. (See 'Primary hypertension' above.)

•Secondary HTN, in which an underlying cause is identified (table 5). (See 'Secondary hypertension' above.)

The most common condition resulting in secondary HTN is kidney disease, followed by endocrine and renovascular diseases. Rarely, monogenic disorders, such as glucocorticoid-remediable aldosteronism, autosomal polycystic kidney disease, and Liddle syndrome, can cause HTN. (See 'Secondary hypertension' above.)