EVALUATION OF THE RENIN-ANGIOTENSIN PATHWAY IN PAEDIATRIC HYPERTENSION
Keywords:
Paediatric Hypertension, Renin-Angiotensin System, Aldosterone, Angiotensin II, Target Organ Damage, Genetic MutationsAbstract
This study aimed to evaluate the renin-angiotensin pathway in paediatric hypertension, with the objective of understanding its biochemical, clinical, and genetic associations in children aged 6 to 18 years. Using a cross-sectional design, 84 participants (42 hypertensive and 42 normotensive) were recruited from a tertiary paediatric cardiology and nephrology clinic. Comprehensive clinical data, ambulatory blood pressure monitoring, biochemical analyses, imaging studies, and genetic testing were performed. The hypertensive group demonstrated significantly elevated levels of plasma renin activity (12.5 ± 3.2 ng/mL/hr), serum aldosterone (25.7 ± 6.4 ng/dL), and angiotensin II (182 ± 29 pg/mL) compared to the normotensive group (p < 0.001). According to the clinical tests, hypertensive children demonstrated the body mass index (22.8 ± 4.5 kg/m²), increased left ventricular mass index (49.2 ± 8.6 g/m²), and high albumin-to-creatinine ratio in the urine (134 ± 32 mg/g), Structural renal abnormalities were identified in 38% of hypertensive children through diagnostic imaging and findings suggestive of cardiac remodeling in the form of echocardiographic pictures were seen in 41%. 30% of cases with familial hypertension have mutations in the SCNN1B, CYP11B2 and WNK1 genes revealed by genetic testing. Ambulatory monitoring revealed nocturnal hypertension in 64% of hypertensive group, which highlights the need to prolong the assessment of blood pressure in children. These findings demonstrate the key role of the renin-angiotensin system in paediatric hypertension and its relation to target organ damage and genetic predisposition. Imaging and biochemical assessments at the same time, coupled with genetic screening, can improve diagnostic accuracy, and facilitate personalized approaches to therapeutics in paediatric hypertensive populations.
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Copyright (c) 2025 Muska Hayat , Sami Ullah, Shahzad Rafiq (Author)

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