INTRODUCTION — It has become clear that hypertension (HTN) begins in childhood and adolescence and that it contributes to the early development of cardiovascular disease (CVD) in the 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. (See "Overview of risk factors for development of atherosclerosis and early cardiovascular disease in childhood", section on 'Hypertension'.)
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 upon these observations, identifying children with HTN and successfully treating their HTN should have an important impact on long-term outcomes of CVD.
The epidemiology, risk factors, and etiology of childhood HTN will be reviewed here. The diagnosis, evaluation, and treatment of HTN in children and adolescents are reviewed separately. (See "Definition and diagnosis of hypertension in children and adolescents" and "Evaluation of hypertension in children and adolescents" and "Nonemergent treatment of hypertension in children and adolescents".)
Neonatal HTN, including etiology, is also discussed separately. (See "Etiology, clinical features, and diagnosis of neonatal hypertension".)
DEFINITION — 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 upon sex, age, and height (table 2 and table 3).
A more complete discussion on the classification of BP, and the definition and diagnosis of HTN in children and adolescents is found separately. (See "Definition and diagnosis of hypertension in children and adolescents", section on 'Definition'.)
Childhood HTN is also divided into two categories depending upon 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.
EPIDEMIOLOGY — In the United States, the reported prevalence of HTN for adolescent participants (ages 12 to 19 years) in the 2001 to 2016 National Health and Nutrition Examination Survey (NHANES) and as defined by the 2017 American Academy of Pediatrics (AAP) guidelines declined from 7.7 to 4.2 percent [2]. This decline was seen in all weight status categories.
This prevalence of 4 percent for pediatric hypertension was also noted by a systematic review and meta-analysis of studies conducted in many different countries and parts of the world, including both rural and urban populations [3]. This study used a strict definition of hypertension, 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 is dependent upon the definition used to categorize BP. Several studies reported increased 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 (ESH) guidelines [2,4-10]. 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, male and individuals who are overweight or obese were more likely to be reclassified with a higher category of BP (ie, elevated BP or HTN) [2,4,6]. 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 obese adolescents with type 2 diabetes (13 versus 8 percent) [11].
RISK FACTORS FOR PRIMARY HYPERTENSION — Risk factors for primary HTN can be separated into modifiable and nonmodifiable factors.
Modifiable risk-factors
Dietary sodium intake — Observational data have shown that BP levels in children increase with higher sodium intake:
●Analysis of the US NHANES (National Health and Nutrition Examination Survey) data after controlling for both overall and central obesity demonstrated an increase in systolic elevated BP for children with an elevated sodium intake (defined as >1.5 x RDI [reference daily intake]) compared with those with a lower sodium intake (<1.5 x RDI)(odds ratio [OR] 1.36; 95% CI, 1.04-1.77) [12].
●A meta-analysis reported an increase of 6.3 mmHg (95% CI, 2.9-9.6) for systolic BP and 3.5 mmHg (95% CI, 1.2-5.7) for diastolic BP for every additional g of sodium intake in children with elevated BP [13].
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 [14]. (See "Cardiovascular consequences of obstructive sleep apnea in children", section on 'Changes in blood pressure'.)
One observational study reported improvement in sleep disorder was associated with improved BP control [15]. Another study suggested that adenotonsillectomy for OSA in children who are not obese was associated with lower BP [16].
Obesity — There is strong observational data linking the risk of HTN to obesity and being overweight in school-aged children [12,17-21]. By contrast, a report from the Bogalusa Heart study showed that mean systolic and diastolic 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 [22]. Nevertheless, within this cohort of 11,478 children, there was a positive correlation of 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, as illustrated by the following studies:
●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 [23].
●In a prospective study, SBP and weight-for-length were measured in 530 children from birth to three years of age [24]. An increase in the weight-for-length in the first six months of life was associated with higher SBP at three years of life, particularly among infants who were thin at birth.
●In a study of preschool-aged children, after adjusting for age and sex, overweight/obese children who did not meet the daily exercise goal (60 minutes of moderate to vigorous activity) were three times more likely to have an elevated SBP compared with nonoverweight children who met the daily exercise goal [25].
Breastfeeding — There are reports that breastfeeding is associated with lower BPs in childhood, as illustrated by two prospective cohort studies [26-28]. (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 [26]. 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 SBP reduction increased with the duration of breastfeeding.
●Similar findings were found in 7223 singleton infants evaluated at five years of age [28]. Those who were breastfed for six months had SBP that was 1.2 mmHg lower than in infants who had been breastfed less than six months or not at all [28].
White coat hypertension — White coat or isolated office HTN is defined as office BP readings ≥95th percentile but with normal values outside the clinical setting. Studies suggest a prevalence as high as one-third to one-half of children being evaluated for persistently elevated casual BP [29,30].
It is possible that white coat HTN in children represents two populations: one that is destined to develop primary HTN (prehypertensive) [31,32] and one that remains normotensive outside the clinical setting. In adults, white coat HTN appears to be a prehypertensive condition with increased left ventricular mass and progression to sustained HTN. Similar findings were noted in a retrospective study of children with white coat HTN from a tertiary center [33]. Approximately two-thirds of children with white coat HTN had either left ventricular hypertrophy detected by echocardiography or SBP greater than the 95th percentile for age, height, and gender during treadmill exercise. These observations have led to the concern that patients with white coat HTN are at risk for developing HTN and end-organ cardiac damage [30].
Masked hypertension — Masked hypertension is characterized by normal BP in clinic or office and a high ambulatory BP outside of the office, including home. Masked hypertension is reported to have cardiovascular risk similar to sustained hypertension [34]. Diagnosis of masked hypertension is typically made by ambulatory BP monitoring and it should be suspected in children with previously elevated clinic BP readings, lack of correlation between clinic BP and evidence of end organ damage, and obese individuals [35]. Current guidelines recommend performing ABPM at least yearly to assess for masked hypertension in children and adolescents with history of CKD and hypertension [1]. (See "Ambulatory blood pressure monitoring in children", section on 'Masked hypertension'.)
Tobacco exposure — Both active and passive tobacco exposure appears to increase BP. This was illustrated by a multivariate analysis of data from 2007-2016 NHANES of 8520 children (mean age 13.1 years) that reported 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) [36]. (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 increase mortality and morbidity in the adult life. Observational data have linked childhood adverse events with increased risk of overweight and obesity, cardiovascular disease (coronary heart disease and stroke) and hypertension [37-39]. In a systematic review of 30 articles, Sugilia et al reported a consistent positive correlation between violence experienced during childhood and cardiovascular, outcomes, including hypertension [38], Adverse Childhood Events (ACEs) scale is a composite measure for adversities such as abuse, neglect, and parental divorce. In a study, Su and colleagues reported that after the age of 30 years, faster increases in systolic and diastolic BP were seen in individual with multiple ACE exposures when compared with those with fewer ACE exposures [39].
Prenatal and neonatal factors — There is increasing evidence that prenatal and neonatal factors contribute to higher BP [40]. There are data demonstrating a role for low birth weight (BW) in the development of primary HTN (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 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) [41].
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 that found no difference in BP or the rate of chronic kidney disease (CKD) progression between patients with an abnormal birth history (BW <2500 g, gestational age <36 weeks, or small for gestational age) and those with a normal birth history [35].
Non-modifiable risk factors
Sex — In the United States and Canada, the prevalence of HTN and prehypertension is greater in boys than girls [17,20]. In a Canadian cohort study of adolescents, boys were more likely to have high SBP (>90th percentile) compared with girls in 7th (OR 1.29, 95% CI 0.77-2.16), 9th (OR 1.98, 95% CI 1.35-2.93), and 11th grades (OR 2.74, 95% CI 1.52-4.94).
Race — Data from NHANES III showed that the incidence of HTN in adults was affected by race and ethnicity, being most common in non-Hispanic Black Americans (figure 1A-B) [42].
In the United States, data also suggest that the risk of HTN is greater in Black and Hispanic children compared with White and Asian children dependent on racial background [17,43-45].
●In a study using NHANES data, the prevalence of high BP (greater than the 95th percentile) was 4.6, 4.2, and 3.3 in Mexican American, Black, and White children, respectively, during the study period of 1999 to 2002 [17].
●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 [45]. However, the highest rate of HTN was in White adolescents with obesity (7.4 percent).
●In a study 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 upon two clinic visits was greater in Black girls compared with White girls (5 versus 2.1 percent) when measured at annual visits through age 18 to 19 years [44]. The incidence increased to 10.5 and 3.8 percent in Black and White girls, respectively, whose BMIs were greater than the 95th percentile, and was lower in those with normal BMI (<85th percentile, 3.5 versus 1.7 percent).
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 [46]. In particular, early-onset (age <45 years) and not late-onset parental HTN (≥65 years) is associated with HTN in offspring [47].
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 [48,49] and as much as 60 to 70 percent of HTN in families [50]. (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 [51].
●There is no significant BP correlation between parents and adopted children [52,53].
●Most studies in twins have shown BP correlation is stronger between identical (monozygotic) twins than between fraternal (dizygotic) twins or siblings [51,54]. However, the observation that the BP correlation is stronger among dizygotic twins than other first-degree relatives indicates a nongenetic environmental effect [55].
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".)
ETIOLOGY — Causes of childhood HTN are separated into two classes (table 4):
●Primary HTN – No underlying cause is identified.
●Secondary HTN – An identifiable cause is determined. In children with secondary HTN, the underlying disorder may be curable with complete resolution of HTN.
Primary hypertension — Primary HTN is the most common pediatric cause of HTN and is a diagnosis of exclusion. It is more likely in school-aged children and adolescents who have a family history of HTN, and are overweight or obese. It is also more common in African Americans. (See 'Risk factors for primary hypertension' above.)
Secondary hypertension — There are a number of causes of secondary HTN (table 5), and specific symptoms (table 6) and findings (table 7) may point to a particular disorder. In a Polish review, 351 of 636 children (55 percent) with sustained HTN had a known secondary cause [56]. The most common were renal 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 another observational series, 89 of 132 children (67 percent) with HTN had renal or renovascular disease, 30 (23 percent) had primary HTN, and 13 (10 percent) had nonrenal causes [57]. Glomerulonephritis (GN) and reflux nephropathy were the most common renal cause of HTN in these patients.
The following sections review different etiologies of chronic (ie, persistent) secondary HTN.
Renal parenchymal disease — A variety of intrinsic renal disorders is associated with HTN and includes the following:
●Glomerulonephritis – HTN is a manifestation of acute and chronic glomerular disorders. In children, the most common form of acute glomerular disease is poststreptococcal glomerulonephritis (GN), which follows after a streptococcal infection. Immunoglobulin A (IgA) vasculitis (ie, Henoch-Schönlein purpura) can present with renal manifestations, including HTN. In children, chronic glomerular disorders associated with elevated 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 an elevated serum creatinine or blood urea nitrogen. (See "Overview of hypertension in acute and chronic kidney disease".)
●Renal parenchymal scarring – Renal 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 (HUS) in children", section on 'Hypertension' and "Urinary tract infections in infants older than one month and young children: Acute management, imaging, and prognosis", section on 'Prognosis'.)
●Chronic renal failure (CRF) – CRF of any cause can be associated with HTN because of volume expansion. In addition, children who have undergone renal transplantation are at increased risk for HTN due to several different mechanisms, including rejection or the administration of drugs that increase BP. A functional gene, MYH9, which is expressed in kidney podocytes, has been associated with nondiabetic end-stage kidney disease in Black Americans [58]. (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 — Rarely, monogenic disorders that affect renal tubular function can cause HTN. Several disorders (Liddle syndrome, pseudohypoaldosteronism type 2, glucocorticoid-remediable aldosteronism, congenital adrenal hyperplasia, and syndrome of apparent mineralocorticoid excess) result in increased tubular reabsorption of sodium or chloride, leading to increased vascular volume and HTN. In polycystic kidney disease, the underlying mechanism of HTN is unknown.
●Polycystic kidney disease (PKD) is due to two genetic disorders, autosomal dominant and autosomal recessive PKD, that involve the formation of renal cysts. HTN is a common presenting sign in children with the recessive form of PKD. (See "Autosomal recessive polycystic kidney disease in children".)
●Liddle syndrome (MIM #177220), 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's syndrome and pseudohypoaldosteronism type 1", section on 'Liddle's syndrome'.)
●Pseudohypoaldosteronism type 2 (PHA2), or Gordon syndrome (MIM #145260), 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 renal 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)'.)
●Glucocorticoid-remediable aldosteronism (GRA), also known as familial hyperaldosteronism type I, is a disorder in which there is a chimeric gene formed from portions of the 11beta-hydroxylase gene and the aldosterone synthase gene, which results in adrenocorticotropic hormone (ACTH), stimulating aldosterone synthesis. (See "Familial hyperaldosteronism".)
●Congenital adrenal hyperplasia (CAH) due to 11beta-hydroxylase deficiency 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 (AME, MIM #218030) arises from mutations in 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 renal 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 [59]. (See 'Definition' above.)
Causes of renovascular disease in children include the following:
●Fibromuscular dysplasia – Fibromuscular dysplasia is the most common etiology of renovascular disease [60,61]. 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 [62]. (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 causes of renovascular disease include neurofibromatosis, arteritis, renal artery hypoplasia, and midaortic syndrome (segmental narrowing of the proximal abdominal aorta) [60,61,63]. (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 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 ACTH. (See "Causes and pathophysiology of Cushing's syndrome".)
•Mineralocorticoid excess that results in HTN may be seen in patients with CAH. Other rare causes of HTN due to mineralocorticoid excess include aldosterone-secreting tumors and the monogenic disorder of GRA. (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 disease'.)
Cardiac disease — Coarctation of the aorta is the primary cardiac cause of HTN. The classic findings are HTN in the upper extremities, diminished or delayed femoral pulses, and low or unobtainable arterial blood pressure 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 side effects of systemic glucocorticoids", section on 'Cardiovascular effects')
●Oral contraceptives (see "Contraception: Hormonal contraception and blood pressure")
●Arsenic (see "Arsenic exposure and 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 5th to 6th 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 10th to 12th 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.)
●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, being overweight or obese, lack of breastfeeding as an infant, exposure (active or passive) to tobacco smoke, and childhood adverse events. In addition, white coat and masked hypertension appear to increase the risk of primary hypertension. (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 hypertension. (See 'Non-modifiable 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 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. (See 'Secondary hypertension' above.)
The most common condition resulting in secondary HTN is renal disease (68 percent), followed by endocrine and renovascular diseases (11 and 10 percent, respectively). Rarely, monogenic disorders, such as glucocorticoid-remediable aldosteronism, autosomal polycystic kidney disease, and Liddle syndrome, can cause HTN. (See 'Secondary hypertension' above.)
