Current Hypertension Reports最新文献

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.

Purpose of review: Use of renin-angiotensin-aldosterone system (RAAS) inhibiting medications is critical in the prevention of cardiovascular disease and kidney function decline in patients with chronic kidney disease (CKD); however, these agents can lead to hyperkalemia, an electrolyte disorder associated with risk of arrythmia, conduction disorders, and increased overall mortality. Discontinuation, or reduction of dose, of RAAS inhibitor therapy in hyperkalemic patients with CKD can lead to loss of kidney and cardiovascular protection afforded by these medications. Given the high prevalence of hyperkalemia among patients with CKD utilizing RAAS inhibitors, clear management principles are critical to minimize risk and maximize benefit when facing this clinical dilemma.

Recent findings: Strategies to mitigate hyperkalemia that do not interfere with optimal RAAS inhibitor therapy should be prioritized when managing potassium elevation in patients with CKD. These strategies include discontinuing non-RAAS inhibitor medications known to cause hyperkalemia, correction of metabolic acidosis, and maximization of medication therapies that lower serum potassium, including diuretics and sodium-glucose cotransporter-2 (SGLT-2) inhibitors. Initiation of potassium exchange resins should also be considered to allow for sustained RAAS inhibitor utilization. An approach which employs multiple strategies concurrently is important to mitigate hyperkalemia and maintain long-term use of RAAS-inhibitors. Persistence of RAAS inhibitor use in patients with CKD is important to slow kidney function decline, delay onset of dialysis or the need for kidney transplant, and prevent adverse cardiovascular outcomes. When hyperkalemia develops among patients with CKD utilizing a RAAS inhibitor, a deliberate effort to reduce serum potassium levels using an approach that allows for continuation of maximally dosed RAAS inhibitor therapy is important. Patient education and engagement in the potassium management process is important for sustained success.

Purpose of review: To conduct a scoping review of articles which examined the impact of COVID-19 on HTN and HTN medication adherence among underrepresented racial/ethnic minorities.

Recent findings: Seven studies were included in this review and impact of COVID-19 was examined at 4 levels: patient, provider, health system and society. The results indicated that patient level factors, such as high unemployment and inequitable access to telemedicine due to society factors- lack of access to high-speed Internet and variation in the offering of telehealth by health systems, were most impactful on adherence. Additionally, provider level clinical inertia may have further impacted adherence to HTN medication. Our review showed that the COVID-19 pandemic did not introduce new barriers but exacerbated preexisting barriers. Ongoing efforts are needed to change policies at the state and local levels to dismantle inequities in underrepresented communities to ensure access to health care with telemedicine to promote health equity.

Purpose of review: This retrospective study investigated factors that influence the occurrence of decreased systolic and diastolic blood pressure including sociodemographic and economic factors, hypertension duration, cigarette consumption, alcohol consumption, duration of smoking, type of cigarettes, exercise, salt consumption, sleeping pills consumption, insomnia, and diabetes. These factors were applied to predict the reality of systolic and diastolic decrease using the machine learning algorithm Naïve Bayes, artificial neural network, logistic regression, and decision tree.

Recent findings: The increase in blood pressure, both systolic and diastolic, is very harmful to the health because uncontrolled high systolic and diastolic blood pressure can cause various diseases such as congestive heart failure, kidney failure, and cardiovascular disease. There have been many studies examining the factors that influence the occurrence of hypertension, but few studies have used machine learning to predict hypertension. The machine learning models performed well and can be used for predicting whether a person with hypertension with certain characteristics will experience a decrease in their systolic or diastolic blood pressure after treatment with antihypertensive drugs.

Purpose of review: Strong evidence is evolving that physical exercise prevents hypertension and reduces blood pressure in patients with pre- and manifest HTN. Yet, identifying and confirming the effectiveness of exercise are challenging. Herein, we discuss conventional and novel biomarkers such as extracellular vesicles (EVs) which may track responses to HTN before and after exercise.

Recent findings: Evolving data shows that improved aerobic fitness and vascular function as well as lowered oxidative stress, inflammation, and gluco-lipid toxicity are leading biomarkers considered to promote HTN, but they explain only about a half of the pathophysiology. Novel biomarkers such as EVs or microRNA are providing additional input to understand the complex mechanisms involved in exercise therapy for HTN patients. Conventional and novel biomarkers are needed to fully understand the integrative "cross-talk" between tissues to regulate vasculature physiology for blood pressure control. These biomarker studies will lead to more specific disease markers and the development of even more personalized therapy in this field. However, more systematic approaches and randomized controlled trials in larger cohorts are needed to assess exercise effectiveness across the day and with different exercise types.