Metabolic syndrome as risk factor for left ventricular hypertrophy in children with chronic kidney disease.

Background: The metabolic syndrome (MS), a cluster of clinical and biochemical abnormalities including insulin resistance, dyslipidemia and hypertension, is often diagnosed in chronic kidney disease (CKD) children. Left ventricular hypertrophy (LVH) is a major target organ damage in hypertension and an important cardiovascular risk factor in CKD patients. We aimed to identify the most significant risk factors of LVH in children with CKD. Methods: Children with CKD stage 1-5 were enrolled in the study. MS was diagnosed according to De Ferranti (DF) as ≥3 from 5 criteria. Ambulatory blood pressure measurements (ABPM) and echocardiographic evaluation were performed. LVH was defined as ≥95th percentile of LV mass index related to height and age. Clinical and laboratory parameters included: serum albumin, Ca, HCT, cystatin C, creatinine, estimated glomerular filtration rate (eGFR) based on Schwartz formula, triglycerides, high-density lipoprotein (HDL), proteinuria, BMI standard deviation score (SDS), height SDS, waist circumference, ABPM data. Results: 71 children (28 girls/43 boys) with median age 14.05 (25%-75%:10.03-16.30) years and median eGFR 66.75 (32.76-92.32) ml/min/1.73m2 were evaluated. CKD stage 5 was diagnosed in 11 pts (15.5%). MS (DF) was diagnosed in 20 pts (28.2%). Glucose ≥ 110 mg/dL was present in 3 pts (4.2%); waist circumference ≥75th pc in 16 pts (22.5%); triglycerides ≥ 100 mg/dL in 35 pts (49.3%); HDL < 50mg/dL in 31 pts (43.7%) and BP ≥ 90th pc in 29 pts (40.8%), respectively. LVH was detected in 21 (29.6%) children. In univariate regression the strongest risk factor for LVH was CKD stage 5 (OR 4.9, p=0.0019) and low height SDS (OR 0.43,p=0.0009). In stepwise multiple logistic regression analysis (logit model) of the most important risk factors for LVH in CKD children, only three were statistically significant predictors: 1)MS diagnosis based on DF criteria (OR=24.11; 95%CI 1.1-528.7; p=0.043; Chi2 = 8.38,p=0.0038); 2), high mean arterial pressure (MAP SDS) in ABPM (OR=2.812; 95%CI 1.057-7.48; p=0.038;Chi2 = 5.91, p=0.015) and 3) low height SDS (OR=0.078; 95%CI 0.013-0.486;p=0.006; Chi2 = 25.01, p<0.001). Conclusions: In children with chronic kidney disease LVH is associated with the cluster of multiple factors, among them the components of MS, hypertension, stage 5 CKD and growth deficit were the most significant.

Effects of Puberty on Blood Pressure Trajectories - Underlying Processes.

Puberty is a complex process leading to physical, sexual, and psychosocial maturation. The changes in morphology and organ function during puberty also affect blood pressure (BP) regulation, and as a consequence (BP) values change noticeably, reaching values often higher than after reaching full maturity. In children entering puberty, BP, especially systolic, increases and then reaches adult values by the end of puberty. The mechanisms responsible for this process are complex and not fully understood. Sex hormones, growth hormone, insulin-like growth factor-1, and insulin, whose production increases during puberty, significantly regulate BP through complex and overlapping mechanisms. During puberty, the incidence of arterial hypertension also increases, especially in children with excess body weight. The present paper presents the current state of knowledge regarding the influence of processes occurring during puberty on blood pressure.

Endothelial dysfunction as a factor leading to arterial hypertension.

Hypertension remains the main cause of cardiovascular complications leading to increased mortality. The discoveries of recent years underline the important role of endothelial dysfunction (ED) in initiating the development of arterial hypertension. The endothelium lines the interior of the entire vascular system in the body and acts as a physical barrier between blood and tissues. Substances and mediators produced by the endothelium exhibit antithrombotic and anti-inflammatory properties. Oxidative stress and inflammation are conditions that damage the endothelium and shift endothelial function from vasoprotective to vasoconstrictive, prothrombotic, and pro-apoptotic functions. A dysfunctional endothelium contributes to the development of hypertension and further cardiovascular complications. Reduced nitric oxide (NO) bioavailability plays an essential role in the pathophysiology of ED-associated hypertension. New technologies provide tools to identify pathological changes in the structure and function of the endothelium. Endothelial dysfunction (ED) contributes to the development of arterial hypertension and should be considered in therapeutic strategies for children with hypertension.