Introduction: Adhesion molecules: E-selectin and intercellular adhesion molecule 1 (ICAM-1) are well-established markers of endothelial injury. The aim of the study was to assess the relation between E-selectin and ICAM-1 and clinical and biochemical parameters in children and adolescents with primary hypertension (PH). Material and methods: In 77 patients with PH (15.04 ±2.62 years, 50 boys, 27 girls) we evaluated serum E-selectin, ICAM-1, and selected clinical and biochemical parameters including inflammatory indicators and ambulatory blood pressure monitoring (ABPM). Results: The E-selectin concentration was 55.63 ±26.49 ng/ml and the ICAM-1 concentration was 302.17 ±67.14 ng/ml. E-selectin and ICAM-1 correlated (p < 0.05) with BMI Z-score (r = 0.24, r = 0.29), ICAM-1 also with uric acid (r = 0.35), HDL-cholesterol (r = –0.28), platelet-to-lymphocyte ratio (r = 0.26), and systolic and mean blood pressure variability (r = 0.24, r = 0.24); in boys ICAM-1 correlated with mean platelet volume (r = 0.29). In multivariate analysis the only significant predictor of E-selectin was mean arterial pressure during 24 hours (β = 0.329, 95% CI: 0.012-0.646) and of ICAM-1 – uric acid (β = 0.430, 95% CI: 0.040-0.819). In 27 children with newly diagnosed PH E-selectin correlated negatively with diastolic blood pressure dipping (r = –0.54, p = 0.004) and positively with ambulatory arterial stiffness index (r = 0.51, p = 0.012). Conclusions: Elevated mean arterial pressure and hyperuricemia are risk factors of endothelial damage in paediatric patients with primary hypertension. In children with untreated primary hypertension there may be a relation between endothelial damage and disturbed circadian blood pressure profile.

Our study aimed to evaluate factors affecting circadian BP profile and its association with hypertension-mediated organ damage (HMOD) in pediatric patients with primary hypertension (PH). The study included 112 children (14.7 ± 2.1 age, 79 boys, 33 girls) with untreated PH. Non-dipping was defined as a nocturnal drop in systolic or diastolic BP (SBP, DBP) < 10%, and a nocturnal drop >20% was defined as extreme dipping. The nocturnal SBP drop was 10.9 ± 5.9 (%), and the DBP drop was 16.2 ± 8.5 (%). Non-dipping was found in 50 (44.6%) children and extreme dipping in 29 (25.9%) patients. The nocturnal SBP decrease correlated with BMI Z-score (r = −0.242, p = 0.010) and left ventricular mass index (LVMI) (r = −0.395, p = 0.006); diastolic DBP decrease correlated with augmentation index (AIx75HR) (r = 0.367, p = 0.003). Patients with a disturbed blood pressure profile had the highest LVMI (p = 0.049), while extreme dippers had the highest augmentation index (AIx75HR) (p = 0.027). Elevated systolic and diastolic BP dipping were risk factors for positive AIx75HR (OR 1.122 95CI (1.009–1.249) and OR 1.095 95CI (1.017–1.177). We concluded that disturbed circadian BP profile was common in children with PH and should not be considered a marker of secondary hypertension. A disturbed circadian BP profile may be associated with higher body weight. In pediatric patients with PH, non-dipping is associated with increased left ventricular mass, and extreme dipping may be a risk factor for increased arterial stiffness.

Our study aimed to assess active renin concentration in children with primary hypertension. Thus, we evaluated active renin concentration, clinical parameters, office and ambulatory blood pressure, and biochemical parameters in 51 untreated adolescents with primary hypertension (median: 14.4 [interquartile range—IQR: 13.8–16.8] years) and 45 healthy adolescents. Active renin concentration did not differ between patients with hypertension and healthy children (median: 28.5 [IQR: 21.9–45.2] vs. 24.9 [IQR: 16.8–34.3] [pg/mL], p = 0.055). In the whole group of 96 children, active renin concentration correlated positively with serum potassium and office and ambulatory systolic and diastolic blood pressures. Among children with hypertension, patients with isolated systolic hypertension had lower renin concentration than patients with systolic-diastolic hypertension (26.2 [IQR: 18.6–34.2] vs. 37.8 [IQR: 27.0–49.6] [pg/mL], p = 0.014). The active renin concentration did not differ between patients with isolated systolic hypertension and healthy children. In multivariate analysis, diastolic blood pressure Z-score (beta = 0.238, 95 confidence interval [0.018–0.458], p = 0.035) was the only predictor of active renin concentration in the studied children. We concluded that active renin concentration is positively associated with blood pressure and potassium in children, and diastolic blood pressure was the strongest predictor of renin level. Patients with isolated systolic hypertension may differ from patients with systolic-diastolic hypertension in less severe activation of the renin-angiotensin-aldosterone system.

Background: Circulating calcification inhibitors: fetuin A (FA) and osteoprotegerin (OPG) together with soluble ligand of receptor activator of nuclear factor kappa-B (sRANKL) have been linked to vascular calcifications and arterial damage. This study aimed to evaluate relationships between FA, OPG, sRANKL, and arterial damage in children with primary hypertension (PH). Methods: In this cross-sectional single-center study, calcification inhibitors (FA, OPG, sRANKL) levels were measured in blood samples of 60 children with PH (median age 15.8, IQR: [14.5–16.8] years) and 20 age-matched healthy volunteers. In each participant, peripheral and central blood pressure evaluation (BP) and ambulatory BP monitoring (ABPM) were performed. Arterial damage was measured using common carotid artery intima media thickness (cIMT), pulse wave velocity (PWV), augmentation index (AIx75HR), and local arterial stiffness (ECHO-tracking—ET) analysis. Results: Children with PH had significantly higher peripheral and central BP, BP in ABPM, thicker cIMT, higher PWV, and AIx75HR. FA was significantly lower in patients with PH compared to healthy peers without differences in OPG, sRANKL, and OPG/sRANKL and OPG/FA ratios. In children with PH, FA level correlated negatively with cIMT Z-score and ET AIx; sRANKL level correlated negatively with ABPM systolic blood pressure (SBP), SBP load, diastolic BP load, and AIx75HR; OPG/sRANKL ratio correlated positively with SBP load, while OPG/FA ratio correlated positively with ET AIx. In multivariate analysis, FA was a significant determinant of cIMT (mm) and cIMT Z-score. Conclusions: This study reveals that in children with primary hypertension, arterial damage is related to lower fetuin A concentrations. Graphical

Introduction: Recent evidence suggests that vitamin D plays a role in pathogenesis of arterial hypertension. The aim was to assess vitamin D in children and adolescents with arterial hypertension. Material and methods: In 49 children (14.29 ± 3.17 years) with arterial hypertension we evaluated vitamin D status (according to Polish 2018 Guidelines), serum calcium, phosphorus, parathormone, alkaline phosphatase, office blood pressure, ABPM (including ambulatory arterial stiffness index [AASI]), BMI, GFR, uric acid, lipids and albuminuria. None of the children were supplemented with vitamin D. Results: Mean vitamin D concentration was 19.74 ± 9.68 ng/mL. Vitamin D severe deficiency (0–10 ng/mL) was found in 5 (10.2%), deficiency (> 10–20 ng/mL) in 29 (49.0%), suboptimal concentration (> 20–30 ng/mL) in 17 (34.7%), optimal concentration (> 30 to 50 ng/mL) in 1 (2.0%), and high concentration (> 50 to 100 ng/mL) in 2 (4.1%) children. Vitamin D was higher in spring-summer vs. autumn-winter (21.79 ± 10.19 vs. 15.53 ± 7.08 ng/mL, p = 0.03). Vitamin D correlated with height Z-score (r = 0.39, p < 0.01), BMI Z-score (r = -0.34, p = 0.02), uric acid (r = -0.31, p = 0.04), triglycerides (r = -0.37, p = 0.01), but not with office blood pressure and ABPM parameters except for heart rate (r = -0.38, p < 0.01). In 24 children treated with antihypertensive medications vitamin D correlated with AASI (r = 0.50, p = 0.04). Conclusions: Inadequate vitamin D supply is ubiquitous in children with arterial hypertension. Vitamin D deficiency should be suspected especially in autumn-winter period and among obese and short children. The relation between vitamin D status and ambulatory arterial stiffness index suggests negative influence of vitamin D on arterial wall but requires further investigations. Introduction: Recent evidence suggests that vitamin D plays a role in pathogenesis of arterial hypertension. The aim was to assess vitamin D in children and adolescents with arterial hypertension. Material and methods: In 49 children (14.29 ± 3.17 years) with arterial hypertension we evaluated vitamin D status (according to Polish 2018 Guidelines), serum calcium, phosphorus, parathormone, alkaline phosphatase, office blood pressure, ABPM (including ambulatory arterial stiffness index [AASI]), BMI, GFR, uric acid, lipids and albuminuria. None of the children were supplemented with vitamin D. Results: Mean vitamin D concentration was 19.74 ± 9.68 ng/mL. Vitamin D severe deficiency (0–10 ng/mL) was found in 5 (10.2%), deficiency (> 10–20 ng/mL) in 29 (49.0%), suboptimal concentration (> 20–30 ng/mL) in 17 (34.7%), optimal concentration (> 30 to 50 ng/mL) in 1 (2.0%), and high concentration (> 50 to 100 ng/mL) in 2 (4.1%) children. Vitamin D was higher in spring-summer vs. autumn-winter (21.79 ± 10.19 vs. 15.53 ± 7.08 ng/mL, p = 0.03). Vitamin D correlated with height Z-score (r = 0.39, p < 0.01), BMI Z-score (r = -0.34, p = 0.02), uric acid (r = -0.31, p = 0.04), triglycerides (r = -0.37, p = 0.01), but not with office blood pressure and ABPM parameters except for heart rate (r = -0.38, p < 0.01). In 24 children treated with antihypertensive medications vitamin D correlated with AASI (r = 0.50, p = 0.04). Conclusions: Inadequate vitamin D supply is ubiquitous in children with arterial hypertension. Vitamin D deficiency should be suspected especially in autumn-winter period and among obese and short children. The relation between vitamin D status and ambulatory arterial stiffness index suggests negative influence of vitamin D on arterial wall but requires further investigations.

Experimental studies suggest that periostin is involved in tissue repair and remodeling. The study aimed to evaluate serum periostin concentration as potential biomarker in pediatric patients with primary hypertension (PH). We measured serum periostin, blood pressure, arterial damage, biochemical, and clinical data in 50 children with PH and 20 age-matched healthy controls. In univariate analysis, children with PH had significantly lower serum periostin compared to healthy peers (35.42 ± 10.43 vs. 42.16 ± 12.82 [ng/mL], p = 0.038). In the entire group of 70 children serum periostin concentration correlated negatively with peripheral, central, and ambulatory blood pressure, as well as with aortic pulse wave velocity (aPWV). In multivariate analysis, periostin level significantly correlated with age (β = −0.614, [95% confidence interval (CI), −0.831–−0.398]), uric acid (β = 0.328, [95%CI, 0.124–0.533]), body mass index (BMI) Z-score (β = −0.293, [95%CI, −0.492–−0.095]), high-density lipoprotein (HDL)-cholesterol (β = 0.235, [95%CI, 0.054–0.416]), and triglycerides (β = −0.198, [95%CI, −0.394–−0.002]). Neither the presence of hypertension nor blood pressure and aPWV influenced periostin level. To conclude, the role of serum periostin as a biomarker of elevated blood pressure and arterial damage in pediatric patients with primary hypertension is yet to be unmasked. Age, body mass index, uric acid, and lipid concentrations are key factors influencing periostin level in pediatric patients.