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 Table of Contents  
Year : 2021  |  Volume : 6  |  Issue : 2  |  Page : 59-69

Hypertension in children

Department of Pediatric Nephrology, Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka, Bangladesh

Date of Submission29-Nov-2021
Date of Acceptance20-Dec-2021
Date of Web Publication28-Feb-2022

Correspondence Address:
Prof. Ranjit Ranjan Roy
Department of Pediatric Nephrology, Bangabandhu Sheikh Mujib Medical University (BSMMU), Shahbag, Dhaka 1000,
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/pnjb.pnjb_23_21

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Hypertension in children and adolescents is a major health condition that clinicians frequently overlook. Children should have their blood pressure checked annually beginning at the age of 3, or at each visit if risk factors are present. Secondary etiologies of hypertension are more common in children than adults, with renal parenchymal and renovascular disease being the most common. In youngsters, overweight and obesity are highly associated with primary hypertension. All children newly diagnosed with hypertension should have a history and physical examination to rule out any underlying medical conditions. Other risk factors for cardiovascular disease, such as diabetes mellitus and hyperlipidemia, should be examined in children with hypertension, and a retinal examination and echocardiography should be performed to assess for target organ damage. In children with hypertension, lifestyle adjustments such as weight loss if they are overweight or obese, a nutritious diet, and regular exercise are initially used to address the condition. Children with stage 2 hypertension without a modifiable factor such as obesity, evidence of left ventricular hypertrophy on echocardiography, any stage of hypertension associated with chronic kidney disease, or persistent hypertension despite a trial of lifestyle modifications are more likely to require antihypertensive medications. Angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), calcium channel blockers (CCBs), and thiazide diuretics (thiazide diuretics) are all efficacious, safe, and well tolerated in children.

Keywords: ABPM, hypertension, monogenic hypertension, refractory hypertension

How to cite this article:
Roy RR, Sultana N. Hypertension in children. Paediatr Nephrol J Bangladesh 2021;6:59-69

How to cite this URL:
Roy RR, Sultana N. Hypertension in children. Paediatr Nephrol J Bangladesh [serial online] 2021 [cited 2022 May 27];6:59-69. Available from: http://www.pnjb-online.org/text.asp?2021/6/2/59/338569

  Introduction Top

Hypertension (HTN) has become an epidemic globally. Twenty-five percent of the world population is hypertensive. HTN affects 2%–5% of children aged 10–18 years.[1] One of the leading causes of death is uncontrolled HTN.[2] HTN is the second highest cause of death among all cardiovascular disease risk factors, according to the World Health Organization (WHO).[3] Persistently raised blood pressure (BP), formerly known as prehypertension, is also more common in people who are overweight or obese, ranging from 2.2% to 3.5%.[4],[5] Only around half of the 32.6% of US individuals with HTN are aware of their condition (47%) and only about half (54.1%) have regulated BP.[6] Adolescents with high BP constitute 15% of the population.[7] Higher BP in childhood correlates with higher BP in adulthood.[6],[8]

The prevalence of HTN in obesity is 3.8%–24.8.[4] When compared to normal-weight children and adolescents, there is a fourfold increase in BP among those with extreme obesity (body mass index [BMI] >99th percentile) compared to a twofold increase in those with obesity (BMI 95th–98th percentiles).[8] Obesity is associated lack of circadian dip, with 50% not experiencing the expected nocturnal BP dip.[9],[10],[11]

Obesity is a growing epidemic, in Bangladesh 20% of urban children and 8% of rural children are overweight.[12] HTN is three to four times more common in obese and overweight children, with up to 10%–30% of obese children being hypertensive.[4],[13] CPG (Clinical Paediatric Guideline for Screening and Management of High Blood Pressure in Children and Adolescents of AAP, American Academy of Pediatrics) 2017 from the USA has tremendous learning for the global community.[4] It excluded children with obesity in defining or categorizing HTN compared to the fourth report in 2012. Growing obesity, sedentary lifestyles increase the total load of HTN.[6]

Pediatricians do not routinely measure children’s BP until an apparent cause of HTN is evident; thereby, subclinical HTN remains undiagnosed and unaddressed.[4]

Definition of hypertension

Systolic and diastolic blood more than 95th centile for age, gender, and height measured on three or more occasions in the basal state are HTN.[14] Basal state means complete physical and mental relaxation with 3–5 min rest and sitting in the uncrossed leg.[13]

Risk factors of hypertension[4],[13]

  1. It is more common in socioeconomically disadvantageous people, for example, in the USA it is more common in Hispanic and non-Hispanic African-American children compared with non-Hispanic white children.[15]

  2. Known renal/urological condition predisposes to HTN.

  3. Lifestyle and food habit: more HTN in people with a sedentary lifestyle and fast-food consuming.

  4. Family history: 70% HTN in a family is a direct result of genetics, familial hypercholesterolemia, and familial renal disease.

  5. Low-birth weight (LBW), premature, intrauterine growth retardation (IUGR), and babies born with lower uterine segment cesarean section (LUCS).

  6. Neonatal/infancy: acute kidney injury (AKI) leading to chronic kidney disease by any dire illness such as sepsis, asphyxia, pneumonia, history of NICU stay, and umbilical artery catheterization predisposes to HTN.

  7. Congenital heart disease: coarctation of aorta (CoA) and patent ductus arteriosus (PDA).

  8. Sleep apnea, snoring: obstructive sleep apnea syndrome (OSAS).

  9. Drugs: steroid, cyclosporine A (CsA), intravenous fluid, albumin, pseudoephedrine, and herbal, for example, Ephedra.

  10. Alcohol.

  11. Smoking: by adolescent child and mother during pregnancy.

  12. Caffeine.

  13. Excess salt intake.

  14. Raised intracranial pressure.

  15. Tumor lysis syndrome.

  16. Type 2 diabetes mellitus.

  17. Systemic disease: vasculitis and neurocutaneous syndrome.

  18. Bone marrow/renal transplantation.

  19. Recurrent UTI.

  20. Malignancy.

  21. Sickle cell disease.

Indications of blood pressure measurement

All children age 3 years and older should have their BP measured annually. Children aged <3 years with known risk factors should have BP measured in each visit with a physician.[4]

Method of measurement of blood pressure[16]

It is measured by the following:

  • 1. Auscultatory method (by using a mercury or aneroid sphygmomanometer).

  • 2. Palpatory method.

  • 3. Ambulatory blood pressure monitoring (ABPM).

  • 4. Direct (intra-arterial) or umbilical catheter BP measurement (rare practice).

  • 5. Oscillometric method (on a calibrated machine that has been validated for use in the pediatric population).
    • • Auscultatory method:
      • - It is measured at the right arm with cuff of sphygmomanometer covering 80%–100% and sphygmomanometer must be kept at heart level. Patient must be in the basal state, rested for 3 to 5 min in uncrossed leg.

      • - Ideally, BP should be taken in all four limbs. Upper and lower limb BP vary greatly in coarctation of the aorta, Takayasu’s arteritis, Moyamoya disease, and other vasculitis, even a slight difference occurs between right and left sides in a normal person. Sphygmomanometer should be inflated so that the brachial artery is occluded and the pointer goes above 20–30mm Hg of brachial artery occlusion and then gradually deflated until first tapping appear called Korotkoff 1 (k1), which is systolic BP then tapping muffles (K4) which is diastolic BP for less than 13 years. Further lowering BP will lead to the appearance of Korotkoff 5 (K5), which is diastolic BP in more than 13-year-old children. It is frequently absent and unreliable, so K5 is obtained by adding 12mm Hg with K4.

      • - K1 appears 10–20mm Hg higher than palpatory BP, and 3 mm lower than intra-arterial measured BP.[4]


It is a portable device programmed to measure BP every 15 min during wake hours (08:00 am–22:00 pm), every 30 min during sleep (22:00 pm–08:00 am). It is measured in a child >5 years of age, height >120 cm, to know accurate BP in the difficult situation. Mean systolic and diastolic BP is calculated separately for 24 h, and mean pressure is noted.[1] ABPM is essential to avoid target organ damage by HTN; there are reports of dementia, chronic kidney disease (CKD), left ventricular hypertrophy, and impaired vision by retinopathy caused by episode of undetected HTN in an apparent controlled hypertensive person.[4],[17] This is also needed for confirmation of HTN.

Indication of ambulatory blood pressure monitoring[13],[18]

  • 1. White coat HTN

  • 2. Masked HTN

  • 3. Unusual BP variability or episodic HTN occurs in
    • i. CKD

    • ii. Obesity

    • iii. OSAS

    • iv. History of prematurity, LBW

    • v. Diabetes mellitus

    • vi. Post-transplant

    • vii. Post-coarctation repair

  • 4. Borderline HTN

  • 5. Resistant/refractory HTN

  • 6. Determining the efficacy of drug treatment over 24 h.

  • 7. HTN with modifiable risk factors

  • 8. Apparent drug-resistant HTN

Classification of HTN

CPG (Clinical Paediatric Guideline for Screening and Management of High Blood Pressure in Children and Adolescents) 2017[4]

Click here to view

  • - White-coat HTN: When BP recording is higher in doctors’ place.[4],[13]

  • - Masked HTN: high BP at home but normal at doctor’s place.

  • - Dipping: (mean wake BP––mean sleep BP/mean wake BP) × 100, normal dipping at sleep is 10%, sleep BP < wake BP.

  • - BP index: average BP/95 centile, HTN, if index > 1.

  • - Resistant HTN: persistent HTN with three drugs of different group in maximum dose including one diuretic or BP controlled with four or more medication.

  • - Urgency: HTN with less severe symptoms.

  • - Emergency: HTN with features of its severe symptom and target organ dysfunction.[13]

  • - BP load: BP more than normal value, >25%–30% above normal. Adult HTN, 20% prevalence, has childhood incidence. Children with HTN have 2.5 times the risk of becoming adult hypertensive.[4],[18],[20]


Approximately 75%–90% of pediatric HTN are of renal or renovascular etiology.[13],[21],[22]

Causes are as follows:

  • Acute glomerulonephritis (AGN).

  • AKI.

  • CKD: It comprises 20% of pediatric HTN.[13],[23]

  • Chronic glomerulonephritis (chronic glomerulonephritis [GN]).

  • Renovascular: renal vein thrombosis and renal artery stenosis.

  • Nephrocalcinosis.

  • Hereditary renal disease: nephronophthisis and polycystic kidney disease.

  • Renal vasculitis.

  • Reflux nephropathy.

  • Hydronephrosis.

  • Obstructive uropathy.

  • Pyelonephritis (chronic and recurrent).

  • Hemolytic uremic syndrome.

  • Congenital dysplastic kidney.

  • Multicystic kidney disease.

  • Essential (primary) hypertension[24]

  • Primary HTN is more common in obese and after 6 years.[25],[26]

  • Metabolic syndrome: it is the combination of HTN, obesity, dyslipidemia, and diabetes mellitus.[6] There occurs insulin resistance, salt and water retention, increased renin aldosterone and angiotensin system (RAAS) activation, and increased leptin by adipocyte that causes increased sympathetic activity. Also increased resistance to interleukin-6 (IL-6) occurs.[27]

  • Endocrine

  • Cushing syndrome.

  • Congenital adrenal hyperplasia (CAH).

  • Conn’s syndrome (primary hyperaldosteronism).

  • Pheochromocytoma.

  • Hyperthyroidism.

  • Cardiac

  • CoA.

  • PDA

  • Arteriovenous fistula (large cardiac output [CO] causing increased stroke volume).

  • Middle aortic syndrome: it is characterized by severe narrowing of the abdominal aorta with progressive involvement of the renal and visceral branches.[28]

  • Takayasu’s arteritis.

  • Neurogenic: central nervous system causes hypertension by sympathetic discharge

  • Raised intracranial pressure.

  • Tumor (primary and secondary).

  • Guillain–Barré syndrome (GBS).

  • Autonomic dysfunction.

  • Transverse myelitis.

  • Encephalitis.

  • Poliomyelitis.

  • Medication[29]


    • • Steroid.

    • • Calcineurin inhibitors (CNIs): cyclosporine and tacrolimus.

    • • Erythropoietin.

    • • Albumin.

    • • Excessive saline infusion.

    • • Nonsteroidal anti-inflammatory drugs (NSAIDs).

    • • Vit-D intoxication.

    • • Lead, lithium mercury.

    • • Carbamazepine.

    • • Antidepressants: tricyclic and others.

    • • Antineoplastic: alkylating agent and paclitaxel

    • • Antiemetic.
      • - Metoclopramide.

      • - Prochlorperazine.

    • • Antipsychotic.

      • - Clozapine.

      • - Thioridazine.


  • Amphetamine.

  • Cocaine.

  • Alcohol.

  • Opiate withdrawal.

  • Pregnancy

  • > 12–20-year-old girl.

  • Tumor

  • Wilms’ tumor.

  • Neuroblastoma.

  • Neonate

  • Sepsis and dire illness with AKI leading to CKD.

  • Renal artery stenosis.

  • Bronchopulmonary dysplasia (BPD).

  • Congenital renal disease.

  • CoA.

  • Umbilical artery catheterization.

  • Genetic

  • Gordon syndrome.

  • Liddle syndrome.

  • Apparent mineralocorticoid excess (AME).

  • Turner syndrome.

  • Friedrich’s ataxia.

  • Multiple endocrine neoplasia.

  • William syndrome (hypercalcemia).

  • Neurocutaneous syndrome (genetic)

  • Tuberous sclerosis.

  • Neurofibromatosis.

  • Von Hippel–Lindau syndrome.

  • Autoimmune disease

  • Systemic lupus erythematosus (SLE).

  • Polyarteritis nodosa (PAN).

  • Juvenile idiopathic arthritis (JIA).

  • Goodpasture’s disease (GPA).

  • Mixed connective tissue disorder (MCD).

  • Miscellaneous

  • Pain.

  • Hypercalcemia–calciphylaxis.

  • Pathogenesis[1],[17],[22],[24]

    BP= CO × TPR.

    • • Increased cardiac output: by
      • - Increased volume: sodium and water retention.

      • - Increased renal sodium reabsorption/ decrease excretion.

      • - Increased renin or aldosterone: Renin-angiotensin aldosterone system (RAAS).

      • - Increased insulin.

    • • Increased peripheral vascular resistance: due to

      • - Increased sympathetic activity: increased contractility of vessel.

      • - Increased vascular narrowing, for example, atherosclerosis.

      • - Increased angiotensin II.

      • - Increased endothelin (PGH2).

      • - Decreased endothelial relaxation factors (NO).

    • • Inflammatory endothelial damage mediated by cytokines and chemokines is the central event.

    • • Key event is oxidative stress leading to decreased NO synthesis and hence increased vascular tone and HTN.

    • • Decreased NO normally inhibits endothelial myocyte and hence maintains vasodilatation and nonaggregation of the platelet.

    • • There occurs overproduction of NADPH (NOX) and xanthine oxidase (XO).

    • • Superoxide anions increase vascular cell proliferation, migration, apoptosis, inflammation, and endothelial dysfunction.

    Renin angiotensin aldosterone system[30]

      Renin (JGA)  CA (lungs)

    Angiotensinogen → Angiotensin I → Angiotensin II → Vasoconstriction →↑TPR → ↑ BP

    (JGA: Juxtaglomerular apparatus, CA: converting enzyme)

    • • Aldosterone causes sodium and water reabsorption and hence volume overload and HTN.

    • • Angiotensinogen II: has delayed effect of
      • i. Inflammation,

      • ii. Cardiac hypertrophy,

      • iii. Endothelial damage,

      • iv. Mesangial cell proliferation,

      • v. Fibrosis.

    Hypertension in chronic kidney disease are due to the following:[30]

    • i.Fluid overload.

    • ii.Activation of RAAS.

    • iii.Sympathetic hyperactivity.

    • iv.Endothelial dysfunction.

    • v.Chronic hyperparathyroidism causing calciphylaxis.

    • vi.Decreased renalase.

    • vii.Decreased nitric oxide (NO).
      • • HTN causes CKD progression and cardiovascular mortality.

      • • Sixty-three percent of CKD stage I has HTN and 80% in CKD stage V are hypertensive.[31]

      • • More than 50% CKD has uncontrolled HTN.[32]

    Medication injury

  • EPO increases TPR by reducing vasodilatory effect of NO.

  • Glucocorticoid increases Na and H2O retention.

  • Cyclosporin causes vasoconstriction of afferent arterioles and hyperplasia of JGA causing activation of RAAS, more catecholamines, endothelin-1 precursors, and more Na reabsorption at loop.

  • Renovascular hypertension[33]

    • • It comprises 5%–10% of HTN. It is usually diagnosed after a long delay because BP is infrequently measured in children and high values are generally dismissed as inaccurate.[33] It is often asymptomatic with minimal clues.

    • • Causes of renovascular HTN are as follows:[33]
      • - Fibromuscular dysplasia.

      • - Vasculitis:

  • Takayasu’s arteritis,

  • PAN,

  • Kawasaki disease,

  • Other systemic vasculitis.

    • - Syndromic
      • • Neurocutaneous syndrome, for example, tuberous sclerosis.

      • • William’s syndrome.

      • • Marfan’s syndrome.

    • - Extrinsic compression

      • • Neuroblastoma.

      • • Wilms tumor.

      • • Other tumor compression.

    • - Renal vein thrombosis, for example, in umbilical catheterization.

    • - Renal artery stenosis in transplant.

    • - Radiation.

    Guide to suspect renovascular HTN

    Renovascular HTN is generally very high with systolic measurement greater than 200 mm Hg and 27–126 mm Hg higher than the 95th centile for age, sex, and height.[34]

    • i. Stage II HTN, refractory HTN.

    • ii. Diastolic HTN.

    • iii. Target organ dysfunction:
      • - Brain (10%–15%)

      • - Cardiac failure (7%)

      • - Facial palsy

    Up to two-thirds of children will have evidence of left ventricular hypertrophy, approximately 60% will have hypertensive retinopathy, and 10% can have renal dysfunction.[35]

    • iv. Kidney size discrepancy on ultrasonography (USG).

    • v. Epigastric bruit.

    • vi. Hypokalemia.

    • vii. Increased renin.

    Doppler ultrasound is a good guide. The resistive index is used to measure blood flow in the kidney. Sensitivity and specificity of resistive index for renovascular disease detection are 80% and 54%, respectively.[36]

    The idea of renal scintigraphy with DMSA (99m-Tc-dimercaptosuccinic acid) or MAG3 (99M-Tc-mercaptoacetyltriglycine) before and after angiotensin-converting enzyme inhibitor (ACEI) is exquisite in localizing renal artery stenosis, but in practice, the results are very inconsistent.[37]

    Computed tomography (CT) angiography is used mainly for the detection of disease of the aorta. Accuracy of CT angiography as high as 80%.[38]

    Magnetic resonance angiography (MRA) is currently regarded to be adequate for assessment of the aorta[39] and main renal arteries with very good sensitivities (92%–98%) and specificities (70%–96%).[36]

    Measurement of renal vein renin concentrations is a helpful technique in children, especially with renal artery stenosis that is bilateral, segmental, or both. This measurement can allow the ischemic focus to be localized to one kidney or even a small area of one kidney.[40]

    Despite improvements in many imaging technologies, digital subtraction angiography (DSA) is the most accurate technique for assessing suspected renovascular disease in children.[41]

    Management of renovascular hypertension

    These patients generally present with very high BP, of which slow reduction is essential. After confirmation of HTN, all children should be treated with antihypertensive drugs except ACEI or ARB. For a child to be on six or seven antihypertensive drugs and still have uncontrolled HTN is very common.[33]

    Endovascular intervention

    When BP control is inadequate or is associated with significant adverse effects, endovascular treatment can be attempted.[33]

    In pediatric renal artery stenosis, percutaneous transluminal renal angioplasty (PRTA) with or without stenting is a valuable treatment option.[42]

    Although renal artery stenting in children is controversial, it remains an attractive option when immediate recoil to the original angiographic configuration occurs after PRTA or recanalization.[43]

    The mid-aortic syndrome can contribute to HTN in children with renovascular disease.[28]

    These procedures can delay the need for surgery in certain patients,[44] but there is an increased chance of thrombosis, rupture, or pseudoaneurysm formation.[45]

    When a segmental branch stenosis cannot otherwise be successfully treated, segmental ethanol ablation might be appropriate.[40]

    Where medical treatment and angioplasty failed, surgical intervention is the choice of management for refractory HTN. The surgical intervention can be revascularization (bypass) or nephrectomy.[33]

    In revascularization surgery, the ideal conduit would be autogenous with the potential to grow with the child, but no such graft is available. For bench surgery, the internal iliac artery is a useful conduit. In children whose coeliac axis is not affected by the disease, the splenic artery on the left and the hepatic and gastroduodenal arteries on the left/right can be used for renal revascularization.[46]

    Refractory hypertension

    The prevalence of actual refractory hypertension (RH) is unknown, but estimates range from 2% to 40% in the treated hypertensive population. The white coat effect has been observed in as many as one-third of individuals with apparent treatment resistance, and numerous studies have shown medication nonadherence in 50%–80% of patients with RH diagnosis.[47]

    There is no gold standard for measuring adherence. It can be assessed indirectly by pill counting, medication event monitoring system, patient self-reporting, or prescription refill in a closed pharmacy system.

    Socioeconomic factors, treatment complexity, adverse medication effects, depression, lack of belief in the benefit of treatment, and lack of insight into illness are the potential barrier to adherence.[48]

    Medications should preferentially include low-cost and generic antihypertensive, once-daily medications, and combination antihypertensive formulations should be used when available.[49] Engagement of patients in the candid discussion, improvement of physician-patient’s relationships, using non-accusatory language during interviews can help ensure adherence to drugs.[48]

    Causes of refractory HTN are as follows:

    1. Exclude pseudo resistant by noncompliance (maybe up to 50%–80%).[47]

    2. Chronic kidney disease stage 5 on inadequate renal replacement therapy.

    3. Renovascular HTN.

    4. Monogenic HTN: Liddle syndrome, Gordon syndrome, and AME.

    5. Endocrine HTN.

    Monogenic hypertension

    This form of HTN is uncommon, and the exact pathology is unknown. In a study of select hypertensive children without a known etiology, genetic testing for familial hyperaldosteronism type 1 (FH-1), or glucocorticoid remediable aldosteronism (GRA), confirmed responsible genetic mutations are found in 3% of the population.[50])

    Other monogenic forms of HTN include Liddle syndrome, Gordon syndrome, AME, familial glucocorticoid resistance, and mineralocorticoid receptor activating mutation. All manifest as HTN with suppressed plasma renin activity and increased sodium absorption in the distal tubule.[51]

    Liddle syndrome

    An autosomal dominant condition occurs due to the overactivity of the epithelial sodium channel (ENaC). It predominantly manifests in teenage children with variable polyuria, increased thirst, failure to thrive, and HTN. Therapy consists of salt restriction and potassium supplementation along with antihypertensive.[6]

    Pseudohypoaldosteronism type II (Gordon syndrome)

    Pseudohypoaldosteronism type II (also called Gordon syndrome or familial hyperkaliemia) is an autosomal-dominant form of HTN associated with hyperkaliemia with a normal glomerular filtration rate, and occasionally with increased renal salt reabsorption and acidemia. Mutations in the WNK1 and WNK4 kinase genes, located on human chromosomes 12 and 17, respectively, are the cause of this rare form of HTN.[52] It presents with HTN, hyperkaliemia, and hyperchloremic metabolic acidosis with normal glomerular filtration rate (GFR). Administration of hydrochlorothiazide or frusemide results in the reversal of clinical and biochemical abnormalities.[6]

    Apparent mineralocorticoid excess

    Autosomal recessive condition due to deficiency of renal isoform of enzyme 11 B- hydroxysteroid dehydrogenase. Clinical features closely mimic Liddle syndrome, including polyuria, increased thirst, failure to thrive, and early-onset HTN. Treatment with oral dexamethasone (10–30 mcg/kg/daily) suppresses cortisol secretion.[6]

    Glucocorticoid remediable aldosteronism

    Autosomal dominant inheritance is characterized by aldosterone secretion that is solely under the control of ACTH. The patient presents early in life with HTN, and a strong family history of cerebrovascular disease is present in some families. Treatment with low-dose dexamethasone is beneficial.[6]

    Clinical features[13],[29]


  • Failure to thrive.

  • Seizure.

  • Irritability/lethargy.

  • Dyspnea: Features of left ventricular failure (LVF).

  • Unable to feed.

  • Sepsis like feature.

  • Intracranial bleeding.

  • Apnea.

  • Children

    • - Asymptomatic in mild-to-moderate HTN.

    • - Headache.

    • - Neck pain.

    • - Fatigue.

    • - Blurred vision.

    • - Epistaxis.

    • - Abdominal pain.

    • - Nausea, vomiting.

    • - Weight loss/failure to gain weight.

    Chronic hypertension[21]

    • - Poor sense of well-being.

    • - Poor sleep.

    • - Poor growth.

    • - Restlessness.

    • - Epistaxis.

    Features of underlying disease

    • - CKD features
      • ■Anemia, HTN, growth failure, rickets, features of uremia, and acidosis.

    • - Nephrotic syndrome features

      • ■Proteinuria and generalized edema.

    • - Glomerulonephritis features

      • ■Hematuria, proteinuria, oliguria, azotemia, and HTN.

    • - Vasculitis features.

      • ■Fever, rash, HTN, and other systemic features of vasculitis.

    • - Endocrine disorder features.

    • - Renovascular HTN features.

    • - Metabolic syndrome.

    Clinical clues to secondary hypertension[13]

    Click here to view

  • Virilization: CAH

  • Exophthalmos, sweating, and tachycardia suggest hyperthyroidism

  • Café au lait spots and Shagreen patch in neurocutaneous syndrome

  • Mass: tumor and renomegaly

  • Complications

    (end-organ dysfunction)[13]

  • Heart: LVF and congestive cardiac failure (CCF)

  • Brain: Encephalopathy, stroke, and PRES

  • Retinopathy

  • Nephropathy (AKI and CKD)

  • myocardial infarction (MI) in long term

  • PRES: posterior reversible leukoencephalopathy

  • Evaluation for HTN




    N––Neonatal disease

    S––Symptom and sign

    T––Trends in the family

    E/R––Endocrine and renal

    Investigation is individualized, depending upon clinical clues [Figure 1].
    Figure 1: Evaluation of hypertension[13],[21]

    Click here to view

    • 1. To assess severity and duration of CKD
      • - Complete blood count with peripheral blood film

      • - Biochemistry: serum electrolytes, serum urea, serum creatinine, serum calcium, serum phosphate, 24-h urinary total protein, serum albumin, serum parathyroid hormone, alkaline phosphatase, blood and gas analysis

      • - GFR estimation

      • - X-ray hand and wrist (nondominant hand)

      • - Chest X-ray

      • - Electrocardiogram

      • - Echocardiography

    • 2. To detect causes of GN

      • - Urine routine and microscopic examination

      • - Anti-streptolysin O titer

      • - C3, C4, ANA (antinuclear antibody), and anti-Ds DNA

      • - ANCA (antineutrophil cytoplasmic antibodies)

      • - Renal biopsy

    • 3. To detect CAKUT (congenital anomalies of the kidney and urinary tract)

      • - USG of kidney ureter bladder with mean cystic capacity with post voidal residue

      • - RGU (retrograde urethrography), MCU (micturating cystourethrography), and IVU (intravenous urogram)

      • - Radioisotope scan: DTPA, DMSA, and MAG3

    • 4. Evaluation of metabolic syndrome[4]

      • - HbA1C (glycosylated hemoglobin)

      • - Lipid profile

      • - USG of hepatobiliary system to detect and grading of NAFLD (nonalcoholic fatty liver disease)

    • 5. CIMT (carotid intima-media thickness test): marker of arteriosclerosis in familial hypercholesterolemia

    • 6. Pheochromocytoma: 24-h HMA (homovanillic acid)/VMA (vanillylmandelic acid), spot urine for catecholamine, plasma/urinary catecholamine

    • 7. Renovascular HTN: Doppler study

    • 8. Tumor (central nervous system [CNS]/abdominal): CT/MRI

    • 9. Neuroblastoma: MIBG scan (meta-iodobenzylguanidine scan)

    • 10. Evaluation of end organ damage

      • - Fundoscopy

      • - Echocardiography

      • - Urine analysis and S creatinine

      • - CT scan of brain

  • Hypokalemia, hypochloremia, and metabolic alkalosis are diagnostic of aldosteronism.

  • Suspect monogenic if family history of HTN, hypokalemia, decrease renin, and elevated ARR (aldosterone renin ratio)[4]

  • Management[13]

  • Pharmacological: anti-HTN medication

  • Non-pharmacological

  • Surgical

  • Pharmacological[13]

    Initial choice of drug in children and adolescents: ACEI/ARB, β-blocker, calcium channel blocker (CCBs), diuretics (ABCD or ACD)[20]


    ACEI: It works by inhibiting the conversion of angiotensin I to angiotensin II, a strong vasoconstrictor. ACE-I reduces sympathetic activity, limits aldosterone secretion, and produces vasodilation at the efferent arteriole. These drugs also slow down the breakdown of bradykinin, a vasodilator thought to contribute to its antihypertensive effect.[54] This drug has additional antiproteinuric, and antifibrotic effect.

    ARB: Similar to ACE-I, ARBs also target the RAAS; however, they work by directly antagonizing angiotensin II receptors.

    Diuretics: There are three primary classes of diuretics that target various portions of the renal tubule:

  • Loop diuretics are considered the most potent in action and work by inhibiting the sodium-potassium-chloride transport pump in the ascending loop of Henle.

  • Thiazide diuretics, namely hydrochlorothiazide and chlorothiazide, also inhibit sodium reabsorption but target the distal renal tubules.

  • Lastly, potassium-sparing diuretics, such as triamterene, amiloride, eplerenone, and notably spironolactone, work by antagonizing aldosterone in the distal tubule, producing increased sodium and water excretion while leaving potassium and hydrogen ions behind. The combined natriuretic effect and decrease in extracellular volume allows for a lowering of BP.

  • CCBs: They work as an antihypertensive largely by preventing the inflow of extracellular calcium, which is required for cardiac and vascular smooth muscle contraction. Inhibition of calcium flux at this stage causes peripheral arterial vasodilation, which lowers peripheral vascular resistance and BP. The Clinical Practice Guideline for Screening and Management of High Blood Pressure in Children and Adolescents[4] includes long-acting CCBs as an acceptable first-line monotherapy agent, which primarily includes amlodipine and extended-release nifedipine.

    β-Blockers: They work to reduce BP through both negative inotropic and chronotropic effects, thus effectively decreasing cardiac output. The effect of each particular β-blocker is dependent upon specificity and selectivity to each β-receptor type; atenolol, bisoprolol, and metoprolol are very cardio selective and block only β1 receptors, whereas others such as propranolol may antagonize both β1 and β2 receptors.

    Α-Blockers: They selectively block postsynaptic α1.-adrenergic receptors. They dilate arterioles and veins, thus lowering BP. These drugs can be combined with any of the other antihypertensives in other drug classes

    Centrally acting: it reduces CNS sympathetic discharge.

  • Clonidine stimulates the α2-adrenergic receptor, thus resulting in decreased sympathetic outflow leading to decreased peripheral vascular resistance, heart rate, and BP. It should be reserved for patients unresponsive to two or more of the preferred agents.

  • Methyldopa, also an α-receptor agonist, has been prescribed in children as well despite limited clinical trials to support is use in the pediatric patient population.[55]

  • Vasodilator: it directly acts on vessel.[13]

  • Hydralazine is a direct vasodilator that lowers BP by relaxing the smooth muscle of the arteriolar walls and is commonly used in children with uncontrolled BP who are not responding to other treatments.

  • We use combination of antihypertensives depending upon BP load. It is clinical acumen to know what amount of antihypertensive would be required.

    Specific classes should be used in specific clinical circumstances.[13]

    • • Proteinuric HTN: ARB/ ACEI

    • • AGN/AKI/ congenital heart disease: diuretics

    • • HTN with tachycardia: β-blocker

    • • In case of APSGN higher dose of frusemide (1–12 mg/kg/day) can be used.

    • • Hemodialysis is another modality of treating HTN in CKD.
      • ✓ Drug with long half-life and sustained release preparations are better choices.

      • ✓ One from each group/mechanism of action is good.[4],[13]

    Drugs commonly used in hypertensive crisis[4],[13]

    Hypertensive emergencies (severe symptom with target organ dysfunction/failure) always managed with intravenous drugs.

  • Esmolol/labetalol.

  • Hydralazine.

  • Nicardipine.

  • Sodium nitroprusside.

  • Diazoxide.

  • Both oral and intravenous drugs can be used in hypertensive urgency (HTN with less severe symptom).

  • Clonidine: per oral

  • Fenoldopam (dopamine receptor agonists): intravenous

  • Hydralazine: per oral

  • Isradipine: per oral

  • Minoxidil: per oral

  • Approximately one-fourth to one-third of the desired reduction is made over the first 8 h, next one-fourth to one-third within next 8 h, and gradual normalizing of BP over 24–48 h.[6] Rapid fall of BP may cause breakage of cerebral, renal, and other organ autoregulation and hence may cause organ damage, dysfunction with failure.


  • Useful in primary HTN.

  • It includes healthy diet and healthy life style.

  • Avoid sugar, salt, and fat.

  • Exercise: 40 min/day and 5 days/week decreases SBP by 6.6 mm Hg.

  • Appropriate healthy weight.

  • Optimum sleep.

  • Avoidance of smoking.

  • 1-kg weight loss reduces 1 mm Hg BP.

  • More fruits, vegetables, low fat milk.

  • DASH diet: dietary approach to stop HTN[4],[13]

    • • Decrease sodium.

    • • Increase k. Ca, Mg.
      • - 6–8 serving whole grain.

      • - 4–5 serving fruits.

      • - 6–5 serving of vegetables/day.

      • - Low fat dairy foods.

    DASH diet over 3 months reduces BP by 2.2 mm Hg.

    Exercise over 8 month reduces BP by 4.9 mm Hg.[4],[13]

    Surgical treatment[13]

    Click here to view

    Renal artery stenosis and aneurysm: stenting and clipping.

    CoA: repair.

    Wilms’ tumor: resection.

    Pheochromocytoma: resection.

      Conclusion Top

    Pediatric HTN is a growing issue. BP should be measured in pediatric patient. Disclosure of etiology of HTN is essential. Control and prevention are mandatory.

    Financial support and sponsorship


    Conflicts of interest

    There are no conflicts of interest.

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      [Figure 1], [Figure 2]

      [Table 1], [Table 2]


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