Key result
Genetic determinants account for ~30-60% of pediatric blood pressure heritability, sharing loci with adult hypertension.
Why the study?
Elevated blood pressure and vascular changes are detectable within the first two decades of life, with 30-60% heritability, requiring synthesis of current evidence on the monogenic, polygenic, and epigenetic architecture of pediatric hypertension.
A tiered clinical approach integrating biochemical screening for monogenic hypertension, age-specific polygenic risk stratification, and targeting of reversible epigenetic contributors offers a pathway toward personalized care for pediatric arterial hypertension.
May inform age-specific pediatric BP risk models; extends adult GWAS by confirming moderate genetic overlap.
Arterial hypertension in children and adolescents is no longer an exclusively adult disease: elevated blood pressure and vascular changes are detectable within the first two decades of life, and a substantial proportion of this inter individual variability is genetically determined, with heritability estimates of 30-60%. This review synthesizes current evidence on the genetic architecture of pediatric hypertension across three levels of regulation. First, rare monogenic forms with Mendelian inheritance-caused by mutations in the renin-angiotensin-aldosterone system, renal ion transporters, and adrenal steroidogenic enzymes-present with severe, early-onset, treatment-resistant hypertension and respond to pathway-specific pharmacotherapy once diagnosed. Second, the polygenic architecture of essential hypertension is traced from candidate-gene studies to genome-wide association studies, culminating in the Consortium of Childhood Blood Pressure meta-analysis of 28,425 children, which identified eight loci and only moderate genetic correlation (rg = 0.4-0.7) with adult blood pressure, implying age-specific effects. We discuss the translational potential and limitations of polygenic risk scores derived from childhood data for predicting adult cardiovascular outcomes. Third, epigenetic mechanisms-DNA methylation of obesity- and sodium-transport-related genes, and persistent effects of prenatal tobacco exposure-mediate gene-environment interaction and represent the most therapeutically tractable layer of regulation. Finally, we address the emerging role of pharmacogenetics in guiding antihypertensive therapy. We conclude that a tiered approach integrating clinical suspicion of monogenic disease, polygenic risk stratification, and awareness of reversible epigenetic contributors offers the most promising path toward personalized pediatric hypertension care, while noting the predominance of European-ancestry cohorts as a limitation requiring multi-ethnic validation.
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Sozaeva et al. (2026) conducted a review in Pediatric arterial hypertension. Monogenic mutations, polygenic risk variants, and epigenetic modifications was evaluated. Genetic determinants account for 30-60% of pediatric blood pressure heritability, with childhood GWAS identifying 8 loci showing moderate correlation (rg = 0.4-0.7) with adult blood pressure.
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