Current Hypertension Reports最新文献

Purpose of review: This review aims to explore the role of microvascular dysfunction in obesity-hypertension, discuss the effects obesity has on renal microvasculature, review the current methods for assessing microvascular dysfunction and available therapeutic options, and identify critical areas for further research.

Recent findings: There is a strong association between obesity and hypertension. However, the pathophysiology of obesity-hypertension is not clear. Microvascular dysfunction has been linked to hypertension and obesity and could be an important mediator of obesity-related hypertension. Newer therapies for hypertension and obesity could have ameliorating effects on microvascular dysfunction, including GLP-1 agonists and SGLT-2 inhibitors. There is still much progress to be made in our understanding of the complex interplay between obesity, hypertension, and microvascular dysfunction. Continued efforts to understand microvascular dysfunction and its role in obesity-hypertension are crucial to develop precision therapy to target obesity-hypertension.

Purpose of review: The incidence of hypertensive disorders of pregnancy (HDP), especially preeclampsia has increased significantly over the last two decades. Patients with these disorders often report cerebral and visual symptoms, which are listed as potential diagnosis criteria for preeclampsia, if accompanied by new-onset hypertension. Recent studies indicate that cerebral complications in HDP patients are associated with a compromised blood-brain barrier (BBB). The purpose of this review is to highlight the recent literature focused on the BBB in HDP, identify gaps in knowledge, and discuss future directions in this research area.

Recent findings: Majority of the studies addressing BBB changes in HDP are focused on preeclampsia. Recent studies show that hypertension induces increased association of perivascular macrophages/microglia to the cerebral vessels, increased circulating extracellular vesicles, and decreased autoregulation of cerebral blood flow. There is a critical need for more animal studies targeted to protecting the BBB and preventing cerebrovascular complications in the context of HDP. More clinical studies are needed that investigate both the short- and long-term interplay between each HDP subtype and BBB and cognitive function.

Purpose of review: Review parenteral therapeutic choices in treatment of hypertensive crises by mechanism of action and summarize recent literature on the management of hypertensive crises.

Recent findings: Recent data have documented the safety and efficacy of labetalol and nicardipine in treatment of hypertensive crises as well as characterized the hypertensive emergency population to a much greater extent. Based on recent data, hypertensive emergencies are seen in 0.5% of all emergency room visits. Ischemic stroke and heart failure/pulmonary edema are the most common forms of organ damage seen in hypertensive emergencies. There are many therapeutic choices in treatment of hypertensive crises with varied mechanisms of action. Large randomized, controlled trial evidence is lacking in this therapeutic area; however, recent data have documented the safety and efficacy of labetalol and nicardipine.

Purpose of review: Primary aldosteronism (PA) is a leading global cause of secondary hypertension. Subtyping diagnosis of PA is the key to surgery, but accurate classification of PA is crucial but challenging in clinical diagnosis and treatment. The purpose of this review is to provide a summary of current literature and propose subtyping diagnosis flow chart to help us classify PA quickly and accurately.

Recent findings: Early diagnosis and accurate typing are essential for the timely treatment and appropriate management of PA. For most patients, adrenal venous sampling (AVS) is the central choice for typing diagnosis, but AVS is invasive and difficult to promote effectively. CT can help identify unilateral typical adenomas in select patients to avoid AVS. New radionuclide imaging has shown value in the diagnosis and classification of PA, which distinguishes adrenocortical hyperplasia from adenoma and can replace AVS in some patients. Accurately diagnosing unilateral PA is crucial for determining the appropriate treatment strategy for PA. The simple flow chart of PA subtyping diagnosis based on the current literature needs to be verified and evaluated by follow-up researches.

Purpose of review: To review the current literature on care of hypertension and chronic kidney disease for people who are currently and formerly incarcerated, and to make recommendations for improving outcomes.

Recent findings: There is a growing body of literature describing care for kidney disease and hypertension for incarcerated and formerly incarcerated individuals that documents the provision of care itself, notably that many jails contract with private companies; the system is not designed to provide sustained, chronic disease care; and the transition from incarceration to community is fraught with gaps in care. However, deficiencies in data collection and regulation still limit our understanding of the quality of care provided in jails and prisons. Furthermore, more data is needed to understand the impact of structural racism in the criminal legal system on overall disparities in care for hypertension and kidney disease. Insurance coverage rates for people who were formerly incarcerated continue to be lower than the general population despite Medicaid expansion in many states. There is little recent data regarding kidney replacement therapy for this population despite known variation in dialysis modalities and transplant programs by state. Transitions clinics, which connect people who were formerly incarcerated with care in the community upon release, are growing and are important avenues by which to deliver care. People who are incarcerated are disproportionately affected by hypertension and kidney disease, yet data regarding the extent of these inequities and availability of quality care is lacking. More work is needed to understand the care of individuals with kidney disease and hypertension in prisons and to improve outcomes for these common chronic conditions. Both providing effective treatment of kidney disease and hypertension in prisons and jails and providing coordinated, quality transition to community care upon release represents an important opportunity for reform in care for a marginalized population.

Purpose of review: The role of the gut microbiota in modulating blood pressure is increasingly being recognized, currently. The purpose of this review is to summarize recent findings about the mechanisms involved in hypertension with regard to the phenomenon of "gut dysbiosis."

Recent findings: Gut dysbiosis, i.e., the imbalance between the gut microbiota and the host, is characterized by a disruption of the tight junction proteins, such as occludins, claudins, and JAMs (junctional adhesion molecules), resulting in increased gut permeability or the so called "leaky gut." Due to the influence of genetic as well as environmental factors, various metabolites produced by the gut microbiota, such as indole and p-cresol, are increased. Thereby, uremic toxins, such as indoxyl sulfates and p-cresol sulfates, accumulate in the blood and the urine, causing damage in the podocytes and the tubular cells. In addition, immunological mechanisms are implicated as well. In particular, a switch from M2 macrophages to M1 macrophages, which produce pro-inflammatory cytokines, occurs. Moreover, a higher level of Th17 cells, releasing large amounts of interleukin-17 (IL-17), has been reported, when a diet rich in salt is consumed. Therefore, apart from the aggravation of uremic toxins, which may account for direct harmful effects on the kidney, there is inflammation not only in the gut, but in the kidneys as well. This crosstalk between the gut and the kidney is suggested to play a crucial role in hypertension. Notably, the brain is also implicated, with an increasing sympathetic output. The brain-gut-kidney axis seems to be deeply involved in the development of hypertension and chronic kidney disease (CKD). The notion that, by modulating the gut microbiota, we could regulate blood pressure is strongly supported by the current evidence. A healthy diet, low in animal protein and fat, and low in salt, together with the utilization of probiotics, prebiotics, synbiotics, or postbiotics, may contribute to our fight against hypertension.

Purpose of review: This narrative review aims to assess the pathophysiology, diagnosis, and treatment of resistant hypertension (RH) in end-stage kidney disease (ESKD) patients on dialysis, with a specific focus on the effect of renal denervation (RDN) on short-term and long-term blood pressure (BP) control. Additionally, we share our experience with the use of RDN in an amyloidotic patient undergoing hemodialysis with RH.

Recent findings: High BP, an important modifiable cardiovascular risk factor, is often observed in patients in ESKD, despite the administration of multiple antihypertensive medications. However, in clinical practice, it remains challenging to identify RH patients on dialysis treatment because of the absence of specific definition for RH in this context. Moreover, the use of invasive approaches, such as RDN, to treat RH is limited by the exclusion of patients with reduced renal function (eGFR < 45 mL/min/1.73 m3) in the clinical trials. Nevertheless, recent studies have reported encouraging results regarding the effectiveness of RDN in stage 3 and 4 chronic kidney disease (CKD) and ESKD patients on dialysis, with reductions in BP of nearly up to 10 mmhg. Although multiple underlying pathophysiological mechanisms contribute to RH, the overactivation of the sympathetic nervous system in ESKD patients on dialysis plays a crucial role. The diagnosis of RH requires both confirmation of adherence to antihypertensive therapy and the presence of uncontrolled BP values by ambulatory BP monitoring or home BP monitoring. Treatment involves a combination of nonpharmacological approaches (such as dry weight reduction, sodium restriction, dialysate sodium concentration reduction, and exercise) and pharmacological treatments. A promising approach for managing of RH is based on catheter-based RDN, through radiofrequency, ultrasound, or alcohol infusion, directly targeting on sympathetic overactivity.

Purposeof review: Female sex hormones have systemic effects unrelated to their reproductive function. We describe experiences of different research groups and our own, on aspects related to the importance of female sex hormones on blood pressure (BP) regulation and salt-sensitivity-mediated BP response and salt sensitivity without alterations in BP, as well as renal sodium handling and interactions with the immune system.

Recent findings: Changes in sodium intake in normotensive premenopausal women cause more BP variations than in men. After menopause, women often develop arterial hypertension (HT) with a profile of sodium sensitivity. Besides, experimental results have shown that in adult rat models resembling the postmenopausal hormonal state induced by ovariectomy, controlling BP is not enough to avoid renal and other tissue infiltration with immune cells, which does not occur when sodium intake is low or normal. Therefore, excess sodium promotes an inflammatory state with the involvement of immune cells. The evidence of activation of adaptive immunity, besides changes in T cell subpopulations, includes changes in sodium transporters and receptors. More studies are needed to evaluate the particular sodium sensitivity of women and its meaning. Changes in lifestyle and sodium intake reduction are the main therapeutic steps. However, to face the actual burden of salt-sensitive HT in postmenopausal women and its associated inflammatory/immune changes, it seems reasonable to work on immune cell activity by considering the peripheral blood mononuclear cell phenotypes of molecules and transport proteins related to sodium handle, both to screen for and treat cell activation.