Excessive sodium chloride (salt) intake significantly contributes to hypertension and cardiovascular diseases, and reducing sodium is a cornerstone of non-pharmacological management of hypertension. Although the antihypertensive effects of sodium reduction are well established, most existing evidence is from office blood pressure (BP) measurements, with limited data available on home BP. We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) to assess the effects of sodium reduction on home BP. We searched PubMed and the Cochrane Library from inception to September 2025 and included 23 RCTs comprising 4110 participants. Sodium reduction significantly reduced home systolic BP (SBP) (mean difference [MD], –3.66 mmHg; 95% confidence interval [CI], –4.86 to –2.45; P < 0.001) and home diastolic BP (MD, –1.40 mmHg; 95% CI, –2.08 to –0.71; P < 0.001). Nine studies that reported morning home BP also showed reduced morning home SBP (MD, –4.06 mmHg; 95% CI, –6.60 to –1.52; P = 0.002). Greater reductions in home SBP were observed in predominantly hypertensive populations than in non-hypertensive populations (P for heterogeneity = 0.003). No significant differences were detected across other predefined subgroups. Sodium reduction interventions were also associated with significant reductions in salt intake, urinary sodium excretion, and the urinary sodium-to-potassium ratio. Quantitative synthesis was not feasible because only a few included studies reported cardiovascular or adverse events. In conclusion, sodium reduction interventions effectively lower home BP, including morning home BP, with a greater impact in hypertensive populations. Thus, reducing sodium is a practical strategy for improving home BP control, particularly in hypertensive populations. This systematic review and meta-analysis of randomized controlled trials showed that sodium reduction interventions significantly lowered home systolic blood pressure (SBP), including morning SBP. No significant differences in BP-lowering effects were detected across various sodium reduction strategies, and digital health approaches may support implementation and adherence. Sodium reduction interventions were also associated with reductions in salt intake, urinary sodium excretion, and the urinary sodium-to-potassium ratio. These findings support major hypertension guidelines, including the Japanese Society of Hypertension Guidelines for managing elevated blood pressure and hypertension 2025 (JSH2025) and the JSH Morning Hypertension Eradication Program Project (Asakatsu BP Action Plan–the Morning Blood Pressure 130 Campaign).
Studies on the association between smoking and out-of-office blood pressure (BP) remain limited. This systematic review and meta-analysis was conducted to evaluate whether out-of-office BP differs between smoking and abstinence periods. We searched PubMed and IchuShi-Web through September 2025 and identified four non-randomized comparative studies (104 participants) that compared ambulatory BP (ABP) between smoking and abstinence periods among current smokers. The abstinence period ranged from 1 day to 1 week. Mean differences (MDs, smoking minus abstinence) and 95% confidence intervals (CIs) were estimated using a random-effects model. During the smoking period, 24-h systolic BP (SBP) (MD: 2.41 mmHg, 95% CI: -0.13 to 4.95), daytime SBP (MD: 3.47 mmHg, 95% CI: -0.41 to 7.36), and nighttime SBP (MD: 1.38 mmHg, 95% CI: -1.91 to 4.68) were not significantly different compared with those in the abstinence period. In contrast, 24-h diastolic BP (DBP) (MD: 2.67 mmHg, 95% CI: 0.72 to 4.62) and daytime DBP (MD: 3.17 mmHg, 95% CI: 1.15 to 5.18) were significantly higher, whereas nighttime DBP was not (MD: 1.00 mmHg, 95% CI: -1.17 to 3.17). Furthermore, 24-h heart rate (HR) (MD: 6.47 beats per minute [bpm], 95% CI: 3.98 to 8.96), daytime HR (MD: 7.19 bpm, 95% CI: 4.59 to 9.79), and nighttime HR (MD: 3.58 bpm, 95% CI: 0.69 to 6.47) were significantly higher. In conclusion, the ABP profile during the smoking period in current smokers is unfavorable compared with that during the abstinence period, providing further evidence to support smoking cessation.
The effects of intensive systolic blood pressure (SBP) control on cardiovascular (CV) and kidney outcomes across different Kidney Disease Improving Global Outcomes (KDIGO) risk categories remain unclear. We performed a secondary analysis of the Systolic Blood Pressure Intervention Trial (SPRINT) and the SPRINT-eligible Action to Control Cardiovascular Risk in Diabetes Blood Pressure (ACCORD-BP) trial. Participants were categorized into low, moderate, and high/very-high KDIGO risk groups. The primary outcomes were composite adverse CV events (defined as nonfatal myocardial infarction (MI), nonfatal stroke, fatal or hospitalized heart failure (HF), and CV mortality) and composite adverse kidney events (defined as a sustained decline in eGFR of ≥ 40% and end-stage kidney disease (ESKD)). We found that intensive BP control reduced the risk of composite CV events (HR 0.68; 95% CI 0.59-0.78), with attenuated benefits in higher KDIGO risk categories (P for interaction = 0.055). This interaction was mainly driven by nonfatal MI and fatal or hospitalized HF (both P for interaction < 0.05). Intensive BP control increased the risk of composite kidney events (HR 1.88; 95% CI 1.52-2.33), mainly in low- and moderate-risk groups rather than in high/very-high risk groups (P for interaction = 0.04). Similar patterns were observed for sustained eGFR decline (P for interaction = 0.03), but not for ESKD (HR 1.05; 95% CI 0.74-1.48; P for interaction = 0.71). The KDIGO risk classification modified the effects of intensive BP control. Balancing CV benefits against potential kidney impacts in patients with different KDIGO risks during intensive BP treatment is recommended. Trial Registration: ClinicalTrials.gov Identifiers: NCT01206062 (SPRINT) and NCT00000620 (ACCORD).
Poor subjective sleep quality and moderate-to-severe depressive symptoms have both been associated with hypertension, but the extent to which depressive symptoms account for the sleep quality-hypertension association remains uncertain, particularly in community-based populations. This cross-sectional study analyzed data from 210,925 adults in the 2018 Korea Community Health Survey. Sleep quality was assessed with the Pittsburgh Sleep Quality Index and categorized as good or poor, while depressive symptoms were measured with the Patient Health Questionnaire-9 and dichotomized at a score of 10 to indicate moderate-to-severe depressive symptoms. Hypertension was defined as a self-reported physician diagnosis. Logistic regression models estimated associations between sleep quality, depressive symptoms, and hypertension, and counterfactual mediation analysis decomposed the association between poor sleep quality and hypertension into direct and indirect components, adjusting for sociodemographic, behavioral, and clinical factors. Poor sleep quality was associated with higher odds of hypertension (total effect odds ratio [OR], 1.119; 95% confidence interval [CI], 1.091-1.146). The natural direct effect remained significant after accounting for depressive symptoms (OR 1.106, 95% CI 1.078-1.133), whereas the natural indirect effect was statistically significant but small (OR 1.012, 95% CI 1.007-1.016), corresponding to a mediation proportion of 10.8% and 14.6% among non-employed participants. These findings suggest that poor subjective sleep quality was associated with hypertension and that moderate-to-severe depressive symptoms statistically accounted for only a modest proportion of the observed association. Because of the cross-sectional design, these findings should be interpreted as exploratory and hypothesis-generating rather than as evidence of temporal or causal relationships.
Evidence guiding treatment selection for patients already receiving long-term antihypertensive therapy remains uncertain, particularly in older adults. We compared long-term outcomes associated with continued use of angiotensin receptor blockers (ARBs) versus calcium channel blockers (CCBs) among older adults receiving sustained antihypertensive therapy. Using linked administrative claims and health examination data from Japan, we conducted a retrospective cohort study of individuals aged ≥65 years who had continuously received either ARBs or CCBs for at least 12 months, with this time point defined as the landmark for follow-up. Discrete-time proportional hazards models with inverse probability of treatment and censoring weights were used to account for confounding and informative censoring. A total of 59,558 individuals (20,028 ARB users and 39,530 CCB users) were included, with a median follow-up of 4.75 years. Sustained ARB use was associated with a lower risk of heart failure hospitalization (hazard ratio [HR] 0.817, 95% confidence interval [CI] 0.758-0.882) and end-stage renal disease (HR 0.162, 95% CI 0.089-0.295). Risks of myocardial infarction and major adverse cardiovascular events were similar between groups, and stroke risk did not differ meaningfully. Blood pressure levels were comparable throughout follow-up. Among older adults receiving long-term antihypertensive therapy, continued use of ARBs was associated with lower risks of heart failure hospitalization and ESRD/dialysis compared with CCBs, despite similar blood pressure control. These findings may inform treatment selection in patients already established on antihypertensive therapy.
Hyperuricemia commonly coexists with hypertension and is associated with increased renal and cardiovascular risk, yet few antihypertensive agents lower serum uric acid. This study compared the urate-lowering effects of sacubitril/valsartan versus valsartan in adults with primary hypertension and asymptomatic hyperuricemia. This single-center, prospective, randomized, open-label clinical trial enrolled adults with mild-to-moderate primary hypertension and fasting serum uric acid ≥ 420 μmol/L from September 2021 to December 2024, with 12 weeks of follow-up. Participants were randomized 1:1 to sacubitril/valsartan 200 mg once daily or valsartan 160 mg once daily. A standardized stepwise add-on protocol with amlodipine was used to achieve blood pressure control. The primary outcome was the change in fasting serum uric acid from baseline to week 12. In the primary intention-to-treat analysis using multiple imputation, treatment-effect estimates were pooled across imputed datasets using Rubin's rules. In the fully adjusted model, sacubitril/valsartan was associated with a greater reduction in serum uric acid at week 12 than valsartan (β = 30.13 μmol/L; 95% CI, 4.33-55.92; P = 0.022). Similar findings were observed in the per-protocol analysis. Blood pressure control at week 12 was comparable between treatment groups, although more participants assigned to valsartan required escalation to amlodipine 10 mg than those assigned to sacubitril/valsartan (17/75 [22.67%] vs. 4/75 [5.33%]; P = 0.008). In adults with primary hypertension and asymptomatic hyperuricemia, sacubitril/valsartan was associated with greater serum uric acid reduction than valsartan over 12 weeks while achieving comparable blood pressure control. These findings suggest that sacubitril/valsartan may have a favorable uric acid profile among hypertensive patients with asymptomatic hyperuricemia. Trial Registration Chinese Clinical Trial Registry: ChiCTR2100050320 ( https://www.chictr.org.cn ). Date of Registration: September 1, 2021.
Very heterogeneous data have been published concerning prevalence and clinical management of Hypertensive Emergencies (HE) and Uncontrolled Hypertension (UH). The aim of our study was to characterize HE and UH patients evaluating: (i) Blood Pressure (BP) management in Emergency Department (ED), the pharmacological treatment and its adherence to guidelines recommendation; (ii) variables associated with the presence of organ damage; and (iii), as an exploratory analysis, the impact of BP on in-hospital mortality. We performed a multicentre (Niguarda Hospital - Milan and Pio XI Hospital - Desio) retrospective study evaluating patients admitted to ED with BP values ≥ 180/120 mmHg during 2017 and 2019. 1838 patients were admitted to the ED with a BP ≥ 180/120 mmHg (0.95% of total admissions) of whom 37.7% were HE and the remaining (62.3%) were UH. The reduction in Systolic and Diastolic BP (SBP/DBP respectively) was similar in HE (40.6/16.9 ± 26.3/17.7 mmHg) and UH (39.3/15.5 ± 22.4/16.0 mmHg). The most used drugs were intravenous furosemide, nitroglycerin, clonidine and labetalol for HE. Age, smoking, heart failure, previous acute coronary syndrome, chronic kidney disease and diabetes mellitus present a positive association HEs while female sex and chronic anti-hypertensive therapies with 2 or more drugs results as protective variables. Finally, regarding the exploratory analysis, BP at ED admission and its management didn't present significant association with in-hospital mortality. In conclusions, our study demonstrated that adherence to guidelines in the management of HE/UH could be further improved.
Preeclampsia is characterized by endothelial dysfunction and angiogenic imbalance driven, in part, by excess soluble fms-like tyrosine kinase-1 (sFLT-1). Building on previous findings demonstrating vascular modulatory effects of cardiac and quercetin glycosides from Dacryodes edulis seeds during L-NAME-induced vascular perturbation, we investigated whether pear seed glycosides (PSG) modulate sFLT-1-mediated endothelial injury in preeclampsia. Endothelial, preclinical, biophysical, pharmacodynamic, and exploratory clinical approaches were integrated to evaluate PSG activity. TGFβ-stimulated HUVECs, an L-NAME-induced rat model of preeclampsia, orthogonal binding assays (SPR/BLI and MST), ligand competition assays, and a multicenter double-blind phase 1-2a exploratory clinical trial were employed. PSG reduced endothelial migration and suppressed αSMA, TNFα, and fibronectin expression in stimulated HUVECs. In preeclamptic rats, PSG attenuated systolic and diastolic blood pressure elevation, reduced inflammatory and cardiovascular injury markers, restored VEGF and placental growth factor (PlGF), and reduced circulating sFLT-1 and the sFLT-1/PlGF ratio. Bioactivity-guided fractionation identified glycosides as the principal active fraction and improved mean birth weight from 2.7 g in untreated preeclamptic dams to 3.5 g, approaching normotensive controls (3.7 g). Orthogonal SPR/BLI and MST assays demonstrated concentration-dependent PSG-sFLT-1 interactions, while competitive ELISA and BLI assays showed inhibition of sFLT-1-mediated sequestration of VEGF and PlGF. PSG additionally restored VEGFR2/KDR, AKT, and ERK signaling in sFLT-1-exposed endothelial cells. In the exploratory clinical trial, 83 participants were randomized following screening of 125 women, with approximately 80% completing follow-up. PSG administration alongside standard care did not reveal major treatment-emergent safety concerns. These findings support further investigation of PSG as a candidate adjunctive strategy targeting angiogenic dysfunction in preeclampsia.
Co-occurring obesity and hypertension is associated with high cardiovascular risk, whereas the prognostic significance of underweight in the presence of hypertension remains uncertain. We examined whether the association between body mass index category and 10-year risk of major adverse cardiovascular events differed across blood pressure categories. Using the Japan Medical Claims Database from 2005 to 2023, we analyzed 6,262,298 adults without prior cardiovascular disease, chronic renal failure, dialysis, or antihypertensive medication use at baseline. Blood pressure was classified as normal (<120 and <80 mmHg), high-normal (120-129 and <80 mmHg), elevated (130-139 and/or 80-89 mmHg), stage 1 hypertension (140-159 and/or 90-99 mmHg), or stage 2/3 hypertension (≥160 and/or ≥100 mmHg). Body mass index was classified as underweight (<18.5 kg/m²), normal weight (18.5-24.9), overweight (25.0-29.9), or obesity (≥30.0). The primary outcome was major adverse cardiovascular events within 10 years. Multivariable Cox proportional hazards models estimated hazard ratios for combined blood pressure and body mass index categories, using normal blood pressure with normal weight as the reference. During a median follow-up of 1,183 days, 34,034 participants experienced major adverse cardiovascular events. Underweight showed a marked blood pressure-dependent increase in risk, with the hazard ratio rising from 1.14 (95% confidence interval, 1.07-1.22) in normal blood pressure to 5.01 (4.23-5.93) in stage 2/3 hypertension. The interaction between blood pressure category and body mass index category was significant. These findings suggest that higher blood pressure may amplify the adverse prognostic significance of underweight.
Circadian blood pressure (BP) values may be different from clinic BP values. Thus, antihypertensive therapy guided solely by clinic BP might not prove appropriate. Moreover, ambulatory BP parameters are superior to clinic BP in predicting outcomes, indicating they should receive more attention as therapeutic targets. Among all relevant 24-h BP parameters, in both untreated and treated patients, two clinically unpredictable windows with proven prognostic relevance deserve attention: the period after awakening and the nighttime one. Some patients exhibit higher BP after awakening, which is associated with increased risk. In untreated patients, underdosed therapy could be started. In treated ones, most likely the drug taken the previous morning could not provide adequate duration of action. In this context, a medication with delayed onset of action and peak effect after several hours added in the evening could be of benefit to blunt morning BP rise. Others show high nighttime BP, which is associated with increased risk. In untreated patients, this can lead to prescribe underdosed therapy. In treated patients, most likely antihypertensive therapy in the morning does not cover the 24-h period. In this context, a drug with rapid onset of action and peak effect after few hours added in the evening could reduce high nighttime BP. Globally, evening therapy must be tailored to nighttime BP pattern to achieve the desired effect in the early morning or during the night. Future studies in which antihypertensive therapy is tailored to circadian BP profile, a more physiological definition of chronotherapy, should be scheduled.
Individuals with chronic kidney disease are at increased risk for herpes zoster, cardiovascular events, kidney failure, and premature mortality. Although the recombinant zoster vaccine effectively prevents herpes zoster, its broader systemic effects in this population remain unclear. We conducted a retrospective cohort study of adults aged 50 years or older with incident chronic kidney disease using the U.S.-based TriNetX network from 2017 to 2024. A total of 13,218 vaccine recipients were propensity score-matched to 13,218 unvaccinated controls. The primary outcome was a kidney event, defined as progression to end-stage kidney disease or initiation of dialysis. Secondary outcomes included cardiovascular events and all-cause mortality. Cox proportional hazards models were used to estimate hazard ratios, with additional analyses of restricted mean survival time over five years and incidence rate differences. After a median follow-up of 3.0 years (IQR, 1.5-4.9), recombinant zoster vaccination was associated with significantly lower risks of kidney events (hazard ratio, 0.63; 95% CI, 0.57-0.70), cardiovascular events (hazard ratio, 0.74; 95% CI, 0.68-0.80), and all-cause mortality (hazard ratio, 0.51; 95% CI, 0.48-0.54). Greater risk reductions were observed among individuals who completed the two-dose series. These findings suggest that recombinant zoster vaccination in patients with chronic kidney disease is associated with substantial and sustained reductions in kidney disease progression, cardiovascular events, and mortality, supporting a potential role for vaccination in long-term cardiorenal protection.
A family history (FH) of hypertension is associated with an increased risk of new-onset hypertension. However, the risk of FH estimated in normotensives using conventional methods may have been somewhat underestimated by excluding early-onset cases, who are highly likely to have FH of hypertension. This large-scale longitudinal study on a middle-aged population (mean age: 46.8 years) revealed that the hazard ratio of FH of hypertension for the development of hypertension was higher when calculated for the entire study population (N = 34,792), including hypertensives at baseline by treating them as left-censored cases, using an interval-censored Cox proportional hazards model (1.73, 95% confidence interval: 1.67-1.79, P < 0.001) than that calculated in normotensives (n = 28,271) using a conventional Cox model (1.35, 95% confidence interval: 1.28-1.44, P < 0.001). The effect of changes in the possible confounders during the follow-up period was negligible. Thus, the risk of FH of hypertension for the development of hypertension may be higher than previously reported.
Cardiovascular health disparities across ethnic groups have been well-documented in adults, but temporal patterns in children and underlying molecular mechanisms remain poorly understood. We analyzed two cohorts: the China Health and Nutrition Survey (CHNS, 1991-2015) with 8,062 children (13.7% minorities) and a contemporary regional Shimian County study (2021-2024) with 3,612 children (32.5% minorities, primarily Yi and Tibetan). We assessed blood pressure, anthropometrics, echocardiographic parameters, and sociodemographic factors. A nested case-control lipidomics study (n = 111) characterized ethnicity-specific molecular signatures. CHNS ethnic minority children demonstrated significantly lower odds of elevated blood pressure compared to Han Chinese (adjusted OR for elevated blood pressure: 0.85, 95% CI: 0.74-0.98, P = 0.028), with Han children exhibiting higher systolic blood pressure (98.3 ± 0.1 vs 97.1 ± 0.3 mmHg, P < 0.001). This association was not evident in the Shimian cohort (adjusted OR: 0.90, 95% CI: 0.76-1.07, P = 0.253). Cardiac structural analysis showed that left ventricular dimensions appeared larger in minority children. After body surface area indexing, ethnic differences in cardiac structure were largely attenuated, with systolic function preserved in both groups. Lipidomic profiling identified distinct ethnic-specific molecular signatures: Han children with hypertension showed diacylglycerol upregulation correlating with cardiac parameters (r = 0.45-0.62, P < 0.05), while in minority children triacylglycerol elevation and phosphatidylethanolamine reduction correlated with vascular function indices, though these associations were largely attenuated after adjustment for BMI z-score. Ethnic-specific lipidomic phenotypes may reflect distinct metabolic contexts of pediatric hypertension that warrant mechanistic and longitudinal investigation.
Distinct blood pressure (BP) trajectories were observed after acute stroke and associated with clinical outcomes. This study assessed fluctuations of mean arterial pressure (MAP) and pulse pressure (PP) and evaluated the prognostic significance of MAP and PP trajectory patterns after acute ischemic stroke. We included 4008 acute ischemic stroke patients from the China Antihypertensive Trial in Acute Ischemic Stroke. Latent class mixed modeling identified distinct MAP and PP trajectories using 37 repeated measurements during the first 7 days. We identified five distinct trajectories for MAP and PP: high, high to moderate, high to low, moderate stable, and low. Compared with low MAP trajectory, the adjusted odds ratios (ORs) or hazard ratio (HRs) (95% CIs) of high trajectory were 1.92 (1.33-2.75) for the primary outcome of death and major disability and 1.87 (1.00-3.47) for the composite outcome of cardiovascular events and all-cause mortality. Furthermore, the high to moderate MAP trajectory remained associated with the primary outcome. The high PP trajectory was associated with increased risks of the primary outcome, recurrent stroke, and cardiovascular events in the primary analyses. The significant relationships were confirmed in subgroup analyses, stratified by clinical features and antihypertensive intervention. Both MAP and PP trajectory patterns were associated with death, major disability, and cardiovascular events after acute ischemic stroke. Patients with high or high to moderate MAP and PP trajectories had elevated risk of unfavorable clinical outcomes.
The developmental origins of health and disease (DOHaD) theory proposes that environmental exposure during critical periods of fetal and early postnatal development induces long-lasting biological changes that shape health trajectories across the lifespan. Hypertension and renal injury are adult-onset conditions associated with developmental programming that may increase the risk of non-communicable diseases later in life. Traditionally, reduced nephron endowment and subsequent glomerular hyperfiltration have been considered the principal mechanisms linking adverse fetal environments to subsequent hypertension and kidney disease. However, this paradigm does not fully explain the delayed onset or heterogeneity of these conditions. Accumulating evidence indicates that epigenetic regulation is a key mechanism by which early-life adversity is recorded. Renal stem and progenitor cells have emerged as cellular substrates for developmental programming, retaining information acquired during organogenesis, and influencing renal and vascular homeostasis later in life. Experimental studies have suggested that fetal malnutrition induces persistent epigenetic alterations in these cells, leading to altered differentiation, impaired repair capacity, and dysregulation of the intrarenal renin-angiotensin system, thereby increasing susceptibility to hypertension and renal injury in adulthood. Additionally, metabolic programming may interact with epigenetic regulation through sustained alterations in mitochondrial function and key metabolites. This mini-review summarizes the current evidence linking developmental programming to hypertension and renal injury, focusing on epigenetic regulation in renal stem and progenitor cells and metabolic alterations observed at the renal tissue level. We also discuss the reversibility, clinical implications for early life surveillance, and future directions for life-course strategies to prevent hypertension and renal injury. Graphical abstract. Developmental programming of hypertension and renal injury: epigenetic and metabolic memory. Adverse early-life environments, including fetal malnutrition, fetal growth restriction, ischemia, and prematurity, may program epigenetic memory in renal stem and progenitor cells and metabolic alterations in renal tissue. Epigenetic-metabolic interactions contribute to persistent abnormalities in renal mesenchymal stem cell (MSC) differentiation, intrarenal renin-angiotensin system (RAS) activation, injury-induced activation of label-retaining cells (LRCs), and endothelial progenitor cell (EPC)-mediated vascular repair. Postnatal nutrition, high salt intake, obesity, kidney injury, and ageing may amplify this vulnerability, promoting adult hypertension and renal injury and increasing long-term susceptibility to CKD. Maternal nutrition and supplementation, early surveillance, and lifestyle intervention represent potentially modifiable windows across the life course.
Losartan has a unique uricosuric property among angiotensin II receptor blockers and may therefore be advantageous in patients with hypertension and hyperuricemia or gout. The study by Xu et al. combined a meta-analysis of placebo-controlled randomized trials with a target trial emulation using UK Biobank data and demonstrated that losartan reduced serum uric acid by approximately 0.3 mg/dL. Although this effect is modest and substantially smaller than that of established uric acid-lowering therapies, it may be clinically relevant when selecting antihypertensive treatment for patients with borderline hyperuricemia, gout risk, or diuretic-associated uric acid elevation. Losartan may partially counterbalance the uric acid-raising effect of thiazide diuretics, but it should not replace appropriate treat-to-target therapy in patients with gout or marked hyperuricemia. The study is limited by the small emulated cohort and the possibility of residual confounding and selection bias. Nevertheless, the consistency of the findings across different analytical approaches supports a genuine uric acid-lowering effect. Future studies should determine whether this biochemical effect translates into fewer gout flares, improved attainment of serum uric acid targets, or reduced cardiovascular and cardiometabolic events. Overall, losartan should be regarded as an effective antihypertensive agent with a modest but favorable uric acid profile. Clinical interpretation of losartan's uric acid-lowering effect in hypertension care. ARB, angiotensin II receptor blocker; RCT, randomized controlled trial; URAT1, urate transporter 1.
In heart failure with reduced ejection fraction (HFrEF) having hypertension, elevated serum adiponectin decreased following guideline-directed medical therapy (GDMT) and comprehensive cardiac rehabilitation (CCR). This reduction was associated with left ventricular ejection fraction (LVEF) improvement, suggesting adiponectin as a potential biomarker of therapeutic effects on cardiac metabolism in hypertensive HFrEF.
