Obesity and hypertension represent serious health issues affecting the pediatric population with increasing prevalence. Hypovitaminosis D has been suggested to be associated with arterial hypertension. Serotonin by modulating nitric oxide synthase affect blood pressure regulation. The biological mechanism by which vitamin D specifically regulates serotonin synthesis was recently described. The aim of this paper is to determine the associations between vitamin D, serotonin, and blood pressure in obese children. One hundred and seventy-one children were enrolled in the prospective cross-sectional study. Two groups of children divided according to body mass index status to obese (BMI ≥95th percentile; n = 120) and non-obese (n = 51) were set. All children underwent office and ambulatory blood pressure monitoring and biochemical analysis of vitamin D and serotonin. Data on fasting glucose, insulin, HOMA, uric acid, and complete lipid profile were obtained in obese children. Hypertension was found only in the group of obese children. Compared to the control group, obese children had lower vitamin D and serotonin, especially in winter. The vitamin D seasonality and BMI-SDS were shown as the most significant predictors of systolic blood pressure changes, while diastolic blood pressure was predicted mostly by insulin and serotonin. The presence of hypertension and high-normal blood pressure in obese children was most significantly affected by vitamin D deficiency and increased BMI-SDS. Dysregulation of vitamin D and serotonin can pose a risk of the onset and development of hypertension in obese children; therefore, their optimization together with reducing body weight may improve the long-term cardiovascular health of these children.

Early and reliable markers of acute kidney injury (AKI) are essential. One such candidate marker of tissue damage is extracellular DNA (ecDNA). The aim of our present study is to describe the unknown dynamics of ecDNA in an animal model of AKI. Glycerol-induced nephropathy was used to model AKI in adult male Wistar rats (n = 93). Blood and urine samples were collected 1, 3, and 24 h after model induction. Total ecDNA and its sub-cellular origin was assessed. In the plasma, total ecDNA and nuclear ecDNA were significantly increased in the AKI group already after 1 h (160% and 270%, respectively, p = 0.02 and p = 0.04). Both nuclear and mitochondrial ecDNA were higher after 3 h (180% and 170%, respectively, p = 0.002 and p = 0.005). Urinary ecDNA concentrations in the AKI group were significantly increased only 24 h after model induction (130% for total ecDNA, p = 0.009; 210% for nuclear ecDNA, p = 0.02; and 200% for mitochondrial ecDNA, p = 0.0009). Our results indicate that plasma ecDNA has the potential to serve as an early and sensitive, albeit non-specific marker of AKI. Further studies should elucidate the source of ecDNA and the dynamics of ecDNA in other animal models of AKI and patients with AKI.

Purpose: In overweight/obese adolescents, asymptomatic hyperuricemia is associated with increased prevalence of metabolic syndrome, its components, and a higher cardiometabolic risk. Whether similar associations exist in lean hyperuricemic adolescents is unknown. Subjects and Methods: In 2424 adolescents (51.9% females) aged 16-19 years, anthropometric variables, blood pressure, uric acid, glucose, insulin, lipid profile, inflammatory markers, and renal function were determined. Continuous cardiometabolic score was calculated. Normouricemic vs hyperuricemic subjects were compared among lean and overweight/obese individuals of both sexes. Results: Females (5.4%) and males (13.3%) presented with hyperuricemia; among them 63% of females and 53% of males were lean. In both sexes, hyperuricemic lean and hyperuricemic overweight/obese adolescents displayed similar uric acid concentrations (eg, males: 455 +/- 30 vs 461 +/- 32 mu mol/L, respectively, p=0.933). Lean normouricemic adolescents manifested significantly lower uric acid levels than their overweight/obese peers (eg, males: 333 +/- 46 vs 357 +/- 41 mu mol/L, respectively, p<0.001). Lean normouricemic and hyperuricemic subjects presented similar cardiometabolic score (eg, males: 2.60 +/- 0.67 vs 2.64 +/- 0.60, respectively, p=0.998); among overweight/obese adolescents those with hyperuricemia displayed higher scores compared with their normouricemic counterparts (eg, males: 3.36 +/- 1.04 vs 4.21 +/- 1.65, respectively, p<0.001). A decision-tree model revealed phenotypes associated with higher uricemia, however, distribution of individuals with hyperuricemia among phenotypes was random. Conclusion: In lean adolescents, hyperuricemia is not associated with cardiometabolic profile indicating an increased risk. Existence of this rather prevalent phenotype remains undetected unless lean and overweight/obese subjects are analyzed separately. Longitudinal studies are needed to elucidate the potential clinical consequences of asymptomatic hyperuricemia in lean subjects in later life.