The relationship between obesity and hypertension is well established both in children and adults. The mechanisms through which obesity directly causes hypertension are still an area of research. Activation of the sympathetic nervous system has been considered to have an important function in the pathogenesis of obesity-related hypertension. The arterial-pressure control mechanism of diuresis and natriuresis, according to the principle of infinite feedback gain, seems to be shifted toward higher blood-pressure levels in obese individuals. During the early phases of obesity, primary sodium retention exists as a result of increase in renal tubular reabsorption. Extracellular-fluid volume is expanded and the kidney-fluid apparatus is resetted to a hypertensive level, consistent with a model of hypertension because of volume overload. Plasma renin activity, angiotensinogen, angiotensin II and aldosterone values display significant increase during obesity. Insulin resistance and inflammation may promote an altered profile of vascular function and consequently hypertension. Leptin and other neuropeptides are possible links between obesity and the development of hypertension. Obesity should be considered as a chronic medical condition, which is likely to require long-term treatment. Understanding of the mechanisms associated with obesity-related hypertension is essential for successful treatment strategies. Hypertension Research (2010) 33, 386-393; doi:10.1038/hr.2010.9Keywords: leptin; obesity; pressure natriuresis; rennin-angiotensin-aldosterone system; sympathetic nervous system INTRODUCTION Obesity is a common disorder that develops from the interaction between the genotype and the environment and involves social, behavioral, cultural, physiological, metabolic and genetic factors. A large number of studies have shown that obesity has an important negative impact on health in a population, leading to the recommendation for general practitioners to have an important function in the management of this condition and of its associated comorbidities such as hypertension, hyperlipidemia and hyperinsulinemia/insulin resistance. The relationship between obesity and hypertension is well established both in adults and children. 1,2 Obese individuals exhibit higher levels of office as well as ambulatory blood pressure (BP) from childhood to old age. Obese subjects display higher BP levels than non-obese individuals even in the normotensive range. The combination of obesity, hypertension and other cardiovascular risk factors significantly increases the probability of adverse cardiovascular outcomes, and raises considerations for aggressive treatment strategies. 3 The mechanisms through which obesity directly causes hypertension are still an area of research. Human and animal studies have elucidated the function of adipose tissue derivatives (adipokines and cytokines), neurohumoral pathways, metabolic functions and modulation of pressor/depressor mechanisms. Although obesity-related hypertension may be the result of a combinatio...

Early increase of soluble urokinase plasminogen activator receptor (suPAR) serum levels is indicative of increased risk of progression of coronavirus disease 2019 (COVID-19) to respiratory failure. The SAVE-MORE double-blind, randomized controlled trial evaluated the efficacy and safety of anakinra, an IL-1α/β inhibitor, in 594 patients with COVID-19 at risk of progressing to respiratory failure as identified by plasma suPAR ≥6 ng ml−1, 85.9% (n = 510) of whom were receiving dexamethasone. At day 28, the adjusted proportional odds of having a worse clinical status (assessed by the 11-point World Health Organization Clinical Progression Scale (WHO-CPS)) with anakinra, as compared to placebo, was 0.36 (95% confidence interval 0.26–0.50). The median WHO-CPS decrease on day 28 from baseline in the placebo and anakinra groups was 3 and 4 points, respectively (odds ratio (OR) = 0.40, P < 0.0001); the respective median decrease of Sequential Organ Failure Assessment (SOFA) score on day 7 from baseline was 0 and 1 points (OR = 0.63, P = 0.004). Twenty-eight-day mortality decreased (hazard ratio = 0.45, P = 0.045), and hospital stay was shorter.

pregnancy-induced hypertension (pIh) complicates 6-10% of pregnancies. It is defined as systolic blood pressure (sbp) >140 mmhg and diastolic blood pressure (dbp) >90 mmhg. It is classified as mild (sbp 140-149 and dbp 90-99 mmhg), moderate (sbp 150-159 and dbp 100-109 mmHg) and severe (SBP ≥160 and DBP ≥110 mmHg). PIH refers to one of four conditions: a) pre-existing hypertension, b) gestational hypertension and preeclampsia (pe), c) pre-existing hypertension plus superimposed gestational hypertension with proteinuria and d) unclassifiable hypertension. pIh is a major cause of maternal, fetal and newborn morbidity and mortality. women with pIh are at a greater risk of abruptio placentae, cerebrovascular events, organ failure and disseminated intravascular coagulation. fetuses of these mothers are at greater risk of intrauterine growth retardation, prematurity and intrauterine death. ambulatory blood pressure monitoring over a period of 24 h seems to have a role in predicting deterioration from gestational hypertension to pe. antiplatelet drugs have moderate benefits when used for prevention of pe. treatment of pIh depends on blood pressure levels, gestational age, presence of symptoms and associated risk factors. non-drug management is recommended when sbp ranges between 140-149 mmhg or dbp between 90-99 mmhg. blood pressure thresholds for drug management in pregnancy vary between different health organizations. according to 2013 esh/esc guidelines, antihypertensive treatment is recommended in pregnancy when blood pressure levels are ≥150/95 mmHg. Initiation of antihypertensive treatment at values ≥140/90 mmHg is recommended in women with a) gestational hypertension, with or without proteinuria, b) pre-existing hypertension with the superimposition of gestational hypertension or c) hypertension with asymptomatic organ damage or symptoms at any time during pregnancy. methyldopa is the drug of choice in pregnancy. atenolol and metoprolol appear to be safe and effective in late pregnancy, while labetalol has an efficacy comparable to methyldopa. angiotensin-converting enzyme (ace) inhibitors and angiotensin II antagonists are contraindicated in pregnancy due to their association with increased risk of fetopathy.

White-coat hypertension (WCH) and masked hypertension have been associated with increased cardiovascular risk in adults. In the current study, we investigated: (a) the prevalence of WCH and masked hypertension in pediatric patients and (b) the association of these conditions with target organ damage. A total of 85 children underwent office blood pressure measurements, 24-h ambulatory blood pressure monitoring, echocardiography and ultrasonography of the carotid arteries. Subjects with both office and ambulatory normotension or hypertension were characterized as confirmed normotensives or hypertensives, respectively; WCH was defined as office hypertension with ambulatory normotension and masked hypertension as office normotension and ambulatory hypertension. WCH was found in 12.9% and masked hypertension in 9.4% of the subjects. WCH was significantly more prevalent in obese subjects, while masked hypertension was only present in non-obese ones. Confirmed and masked hypertensives had significantly higher left ventricular mass index than confirmed normotensives (34.0+/-5.8 g/m(2.7), 31.9+/-2.9 g/m(2.7) and 25.3+/-5.6 g/m(2.7), respectively, P<0.05). White-coat hypertensives tended to have higher left ventricular mass index than confirmed normotensives, but the difference was not statistically significant (27.8+/-5.1 g/m(2.7) versus 25.3+/-5.6 g/m(2.7)). No significant differences were found in the intima-media thickness of the carotid arteries between confirmed normotensives, white-coat hypertensives, masked hypertensives and confirmed hypertensives. WCH and masked hypertension are common conditions in children. Confirmed and masked hypertension in pediatric patients are accompanied by increased left ventricular mass index.