Metabolic syndrome (MS) in children with arterial hypertension (HT) contributes to early cardiovascular organ damage, yet MS definitions vary and overlook abnormalities such as elevated serum uric acid (UA). Our study assessed the prevalence, clinical characteristics, and prognostic value of classical and UA-modified MS definitions in hypertensive children at the Children's Memorial Health Institute in Warsaw, Poland. We included 420 patients aged 10-18 years with HT confirmed by ambulatory blood pressure monitoring (ABPM). All underwent anthropometric evaluation, office BP and ABPM measurements, biochemical testing including UA, and assessment of hypertension-mediated organ damage (HMOD): left ventricular mass index (LVMi), carotid intima-media thickness (cIMT), and pulse wave velocity (PWV). MS prevalence by IDF criteria was 14.5%, including 18.3% in children aged 10-15 and 9.4% in those aged 16-18. MS occurred more often in primary than secondary hypertension (17.7% vs. 5.5%; P = 0.003). Compared with non-MS patients, those with MS had higher triglycerides and LDL, slightly higher fasting plasma glucose (P = 0.061), and lower HDL (P < 0.001). UA levels were higher in primary vs. secondary HT (5.8 vs. 5.2 mg/dl; P < 0.001) and in MS vs. non-MS (6.3 vs. 5.5 mg/dl; P < 0.001). MS was associated with greater cIMT-SDS (1.26 vs. 0.92; P = 0.012) and more frequent left ventricular hypertrophy (42% vs. 29%; P = 0.08). Results were consistent across primary and secondary HT subgroups. Adding UA to the MS definition improved prediction of LVH, increasing agreement from κ = 0.086 to 0.190. MS is common in hypertensive children, particularly those with primary HT. Including UA in MS criteria may enhance prediction of HMOD, especially LVH.

The chronic inflammation and insulin resistance (IR) are implicated in hyperuricemia (HUA) pathogenesis, while their interplay remains inadequately characterised. This study aimed to investigate their independent, interactive, and combined effects on HUA risk and serum uric acid (UA) levels, and to quantify the mediating effect of IR in the Southern Chinese population. A cross-sectional study was conducted among 5307 Chinese adults. The triglyceride-glucose (TyG) index served as an alternative marker for IR, and a modified inflammation (mINFLA) score, comprising white blood cell (WBC) count, platelet (PLT) count, and the neutrophil-to-lymphocyte ratio (NLR), was used to assess systemic low-grade inflammation. The multivariable logistic and linear regression models were employed to explore the associations of the TyG index and mINFLA score with HUA risk and UA levels, and the interaction effects and mediating role of the TyG index were further assessed. Subgroup analyses were stratified by age, sex, and disease status. Among 5307 Chinese adults, a higher TyG index and a higher mINFLA score were significantly associated with an increased HUA risk and elevated UA levels, demonstrating significant dose-response relationships (p for trend < 0.001). A significant interaction was observed between the TyG index and mINFLA score in relation to HUA risk and UA levels. Participants exhibiting both high TyG index and mINFLA score had the highest HUA risk and UA levels. Notably, mediation analysis revealed that the TyG index significantly explained 15.4% of the association between the mINFLA score and HUA risk, and 14.5% of the association with UA levels. Chronic inflammation is an independent risk factor for hyperuricemia, with insulin resistance serving as a key mediating factor. Furthermore, these two factors exhibit a significant joint effect on hyperuricemia risk. These findings underscore the importance of simultaneously considering both insulin resistance and chronic inflammation in hyperuricemia prevention and management.

Sulfonylurea herbicides are among the most extensively applied agents in modern agriculture; however, increasing attention has been drawn to their potential adverse effects on nontarget organisms. In this study, we evaluated the subchronic toxicological impact of the sulfonylurea-based herbicide (Sekator: amidosulfuron and iodosulfuron-methyl-sodium) on renal physiology and hematological health in male rabbits (Oryctolagus cuniculus). Twenty-four animals were randomly allocated into four groups: a control group and three treatment groups receiving oral doses of Sekator at 0.213, 0.426, and 1.066 mg/kg body weight daily for a period of 3 weeks. Biochemical assessments demonstrated significant, dose-dependent elevations in serum urea, creatinine, and uric acid concentrations, accompanied by increased kidney weight, collectively indicating renal dysfunction. After taking a close look at the tissue samples, clear signs of kidney damage were found, like swollen tubes and dead tissue. On the blood side of things, several dominant changes happen: There were drops in the number of red blood cells, hemoglobin, hematocrit, and platelets, which are clear signs of anemia. At the same time, there was an uptick in white blood cells, which suggests some kind of inflammation is going on. All in all, these results strongly show that Sekator has harmful effects on the kidneys and blood in a mammal model. This raises some serious flags about the unexpected risks that sulfonylurea herbicides pose to animals that were not meant to be affected. There is need to dig deeper to figure out how this toxicity works and what it means for the environment and health when people are exposed to these chemicals over time.

Eurycomanol alleviates hyperuricemia-induced cortisol disorders by upregulating SRD5A1 via IKKβ-IκBα-NF-κB-DNMT pathway.

The mechanism of honeysuckle peptides in ameliorating hyperuricemia in mice via the PGC-1α/PPARγ/ABCG2 pathway.

Luteolin-stabilized pickering emulsion for encapsulating Enterococcus hirae: preparation, characterization, and synergistic effects on hyperuricemia.

Renoprotective effects of perennial ryegrass attenuate UA mediated renal damage via modulating gut microbiota and anti-oxidative defense.

Lithocarpus litseifolius leaf extract alleviate hyperuricemia-induced renal injury by regulating uric acid metabolism and inhibiting the AKT/S6K pathway.

Buddleja officinalis Maxim. is rich in flavonoids and polyphenols, which exhibits pronounced antioxidant activity. Given that B. asiatica, a related species, has been noted to inhibit xanthine oxidase (XO) in vitro, the urate-lowering effects of B. officinalis have not been confirmed. Thus, this study aimed to screen the XO inhibition of extracts in vitro and to confirm the most active urate-lowering fraction of B. officinalis in vivo. Ethanol extracts were partitioned into n-hexane (HEX), ethyl acetate (EA), n-butanol (BuOH), and aqueous fractions. The EA fraction of B. officinalis extracts exhibited the highest XO inhibitory activity, with it significantly surpassing that of the other fractions (P<0.05). Consequently, the EA fraction was selected for further in vivo evaluation in a mouse model of hyperuricemia, which was induced through intraperitoneal injection of potassium oxonate (PO, 250 mg/kg/day for 7 days). Mice were divided into six groups, including not treated, PO, PO + allopurinol, and low (PO + EA-L), medium (PO + EA-M), and high (PO + EA-H) EA dose groups. EA fractions of B. officinalis extracts were orally administered 1 hr after PO injection. Compared with in the PO group, the serum uric acid levels were significantly reduced in the PO + EA-M, PO + EA-H, and PO + allopurinol groups (P<0.05). These findings support the potential of B. officinalis as a natural XO inhibitor and an adjunctive supplement for hyperuricemia.

Background: Recent findings indicate that the adverse effects of uric acid (UA) on the coronary arteries contribute to the severity of atherosclerotic disease. Objective: This analysis investigates the relationship between serum uric acid concentrations and the SYNTAX score, quantifying coronary artery disease severity (CAD). Methods: A cross-sectional study took place at Saiful Anwar General Hospital from January 2022 to December 2024. A total of 1156 patients diagnosed with CAD who underwent coronary angiography were chosen for the study. Result: The analysis of uric acid levels led to the classification of participants into two distinct groups: the hyperuricemia group (n = 396) and the normouricemia group (n = 760). The analysis involved comparing the groups in terms of the occurrence of CAD and SYNTAX score while examining gender-specific quartiles of uric acid levels. The clinical baseline data underwent evaluation through suitable statistical methods, and a multivariate logistic regression analysis was conducted to pinpoint independent risk factors for CAD. Conclusion: UA showed a positive relationship with the SYNTAX score in individuals with CAD. It serves as an independent indicator for assessing the extent of coronary artery stenosis and has predictive capabilities Keyword : Coronary Angiography; Coronary Artery Disease; SYNTAX Score; Urid Acid.

Background: Gout and chronic lymphocytic leukemia (CLL) represent distinct hematologic and rheumatologic pathologies; however, their concurrent presentation presents significant diagnostic and therapeutic challenges. Tumor lysis syndrome and chemotherapy-induced hyperuricemia are recognized complications of hematologic malignancies, yet the manifestation of acute gouty arthritis with crystallographic confirmation in CLL patients remains an underreported clinical scenario requiring careful diagnostic stratification. Case presentation: We present a 69-year-old male farmer with newly diagnosed CLL (stage C, Binet classification) admitted for acute left knee arthritis with effusion, left ankle arthritis, and concurrent community-acquired pneumonia (CAP). Clinical examination revealed articular inflammation characterized by pain, swelling, erythema, warmth, and significant joint effusion with documented flexion limitation and positive bulging sign. Musculoskeletal ultrasound demonstrated double contour sign, synovial hypertrophy, and effusion measuring 5.8 cm in the suprapatellar recess with monosodium urate (MSU) crystal deposition confirmed by polarized light microscopy of synovial fluid (5,350 cells/mm³, 40% polymorphonuclear neutrophils, 60% mononuclear cells, positive MSU crystals). Serum uric acid was elevated at 10.6 mg/dL. The patient was successfully managed with colchicine, methylprednisolone, arthrocentesis, and supportive care while maintaining CLL treatment preparedness. Conclusion: This case illustrates the importance of confirmatory synovial fluid analysis and ultrasound imaging in the diagnosis of acute gout in the context of hematologic malignancy. Optimal management requires careful coordination between rheumatology and hematology-oncology services to prevent therapeutic complications and ensure safe chemotherapy initiation in CLL patients with concurrent acute gouty arthritis and hyperuricemia.

Midas touch at the nano-bio interface: Size-dependent attenuation of parathyroid hormone signaling by gold nanoparticles.

Hyperuricaemia is a known cardiovascular risk factor. Several angiotensin receptor blockers, such as losartan, can decrease serum uric acid level, but the effect on serum uric acid of angiotensin receptor neprilysin inhibitor remains unclear. This analysis aimed to investigate the effects of Sacubitril/Allisartan on serum uric acid level in Chinese patients with both hypertension and hyperuricaemia. We performed post-hoc analysis of data from a randomized controlled trial that compared the blood pressure-lowering effect at 12 weeks of treatment with Sacubitril/Allisartan (240 or 480 mg/d) and Olmesartan (20 mg/d). Hyperuricaemia was defined as a serum uric acid concentration exceeding the limit (420 μmol/L in male and 360 μmol/L in female) or patients already on antihyperuricemic drugs. The outcome measures included serum uric acid levels at 12, 24 and 52 weeks of treatment. Of the 1197 randomized patients, 401 (33.5%) patients with both hypertension and hyperuricaemia were included in this analysis. Mean serum uric acid levels at baseline were 441.4 ± 60.3 μmol/L, 430.5 ± 67.1 μmol/L, and 449.9 ± 78.6 μmol/L for the Sacubitril/Allisartan 240 mg, Sacubitril/Allisartan 480 mg, and Olmesartan groups, respectively (P = 0.41). Over the 12-week double-blind treatment period, serum uric acid levels decreased significantly from baseline in both Sacubitril/Allisartan groups compared to Olmesartan (-7.7 μmol/L), with a more pronounced reduction in the 240 mg (-37.7 μmol/L) and 480 mg groups (-43.3 μmol/L). Least square mean changes in serum uric acid reductions were greater with Sacubitril/Allisartan versus Olmesartan, with a difference of -30.0 μmol/L (P = 0.01) for Sacubitril/Allisartan 240 mg and -35.6 μmol/L (P = 0.002) for Sacubitril/Allisartan 480 mg. Treatment with Sacubitril/Allisartan decreased serum uric acid levels significantly more than Olmesartan in Chinese patients with both hypertension and hyperuricaemia, demonstrating a unique uricosuric effect of Sacubitril/Allisartan.

Uricase-based drugs excel at treating refractory hyperuricemia and tumor lysis syndrome by directly degrading uric acid but are limited by immunogenicity. Here, we engineered RAW264.7 macrophages with ectopic co-expression of Aspergillus flavus uricase and murine urate anion transporter 1 (URAT1), forming a "transport-degradation" system: URAT1 actively transports uric acid into cells for intracellular degradation. Recombinant lentiviral vectors carrying target genes were transfected into RAW264.7 cells, followed by puromycin screening. In vitro assays showed that the engineered macrophages nearly completely degraded uric acid (from 556.0 ± 37.0 μmol/L to 0.7 ± 0.6 μmol/L) at 72 h. URAT1 inhibition with benzbromarone abolished uric acid degradation in URAT1-expressing cells. In both acute dietary-induced and chronic genetic hyperuricemic mouse models, RAW-afUri-URAT1 exerted robust and sustained uric acid-lowering activity, maintaining serum uric acid at 77.14 ± 37.48 μmol/L on day 16 in yeast extract gavaged mice and normalizing serum uric acid to 76.2 ± 15.9 μmol/L in liver uricase conditional knockout mice, both significantly superior to the rebound levels observed in mice treated with Rasburicase (143.19 ± 38.21 μmol/L and 142.4 ± 17.4 μmol/L, respectively; P < 0.05). Safety assessments in dietary-induced hyperuricemia mice showed no obvious abnormalities in liver or renal function, and significantly reduced hyperuricemia-related production of inflammatory cytokines (IL-1β, IL-6, TNF-α), Immunogenicity assays showed undetectable anti-uricase antibodies in RAW-afUri-URAT1 treated mice but high level of antibodies in rasburicase treated mice. This engineered macrophage system shows potent, durable uric acid-lowering efficacy, with low immunogenicity and good biosafety, offering a promising strategy for hyperuricemia therapy.

Serum albumin and uric acid: biomarkers of neurocognitive and physical function in early Parkinson's disease.

Serum metabolic markers for α-synucleinopathies conversion in isolated REM sleep behavior disorder: a prospective cohort study.

Background: Serum uric acid (SUA) has emerged as a relevant cardiometabolic and hepatic risk marker in adolescents with obesity. Cinnamon has shown metabolic benefits in adults; however, its effects on SUA and hepatic markers in pediatric populations remain unclear. This study aimed to evaluate the efficacy of cinnamon supplementation on serum uric acid, hepatic enzymes, and lipid profiles in adolescents with obesity. Methods: This is a secondary analysis of a randomized, double-blind, placebo-controlled clinical trial including 93 adolescents (10–18 years) with obesity (BMI ≥ 95th percentile). Participants received either 3 g/day of Cinnamomum verum or a placebo for 16 weeks, alongside lifestyle intervention. Changes in BMI z-score, SUA, alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), and triglycerides were analyzed. Results: The cinnamon group showed a greater reduction in BMI z-score compared to placebo (Δ −0.08 vs. −0.02; p &lt; 0.001). Serum uric acid decreased significantly in the cinnamon group (median change: −0.5 mg/dL [IQR: −1.0 to −0.2]) compared to placebo (−0.1 mg/dL [IQR: −0.4 to 0.2]; p &lt; 0.01). Triglycerides also decreased in the cinnamon group (−18 mg/dL [IQR: −35 to −5]) versus placebo (−5 mg/dL [IQR: −20 to 10]; p &lt; 0.05). Hepatic enzymes (ALT, AST, and GGT) decreased significantly within both groups, without significant differences between groups. In a subgroup of participants with elevated baseline ALT (n = 67), ALT decreased in both groups (placebo: 32.0 to 30.0 U/L, p = 0.004; cinnamon: 33.0 to 26.0 U/L, p = 0.001), with a greater but non-significant reduction in the cinnamon group (Δ −6.0 vs. −2.0 U/L; p = 0.197). Conclusions: Cinnamon supplementation significantly reduced serum uric acid and improved metabolic parameters in adolescents with obesity. These findings suggest that cinnamon may act as an adjunct strategy targeting early cardiometabolic risk markers, particularly uric acid.

Background Diabetic foot ulcers (DFU) as one of the most severe complications of diabetes was characterized by high mortality and incidence of cardiovascular events. Serum uric acid (UA) was well known for cause of gout which was closely related with cardiovascular complications, but also known as the main antioxidant in extracellular fluid. In this study, we aimed to investigate whether serum UA was related with severity and prognosis of patients with DFU. Design and methods 535 patients with diabetes and firstly diagnosed with DFU hospitalized in Ruijin hospital was consecutively recruited. Concentration of serum UA was examined when admission. Participants were grouped into three groups according to tertiles of their serum UA level. These patients were followed up for an average of 48 months to observe the outcomes, including wound healing, non-fatal cerebral and cardiovascular events (NCCE) and all-cause death. The association of serum UA concentration with the severity of disease evaluated through Wagner and Infection degree, and risk of outcomes were analyzed through partial correlation and Cox regression analysis, respectively. Results In bivariate correlation analysis, UA was negatively correlated with the Wagner (r=-0.159, P &amp;lt;0.001) and Infection degree (r=-0.171, P &amp;lt;0.001). In partial correlation, UA was still negatively and independently correlated with the Wagner (r=-0.74, P &amp;lt;0.001) and Infection degree (r=-0.190, P &amp;lt;0.001) after controlling for age, sex, type of diabetes, duration of diabetes, duration of DFU, PAD, HbA1c, serum creatine and urine protein excretion in 24hours. In terms of Cox regression analysis, UA was positively and independently related with the risk of NCCE (HR = 1.002, 1.000 to 1.004, P = 0.011), all-cause mortality (HR = 1.003, 1.001 to 1.004, P = 0.006) and healing rate (HR = 1.001, 1.000 to 1.003,P = 0.042) after adjusting for age, sex, type of diabetes, duration of diabetes, duration of DFU, history of stroke, history of CAD, PAD, HbA1c, serum creatine and urine protein excretion in 24 hours. Conclusion UA might exert a beneficial effect in the context of DFU wound repair, but was an important risk factor for NNCE and all-cause mortality in patients with DFU.

SGLT2 inhibitors reduce urinary protein and slow eGFR decline in clinical trials.However, real-world evidence on within-patient changes in eGFR slope before and after treatment initiation, and their relationship to changes in urinary protein, remains limited.This study was designed to address these concerns. This retrospective study included 90 Japanese CKD patients who initiated dapagliflozin and had ≥ 5 eGFR measurements during both the 12-month periods before and after initiation.The treatment effect was defined as theΔeGFR slope (post-minus pre-initiation slope).Clinical factors associated withΔeGFR slope were assessed using multivariable regression. The mean eGFR slope significantly improved from - 5.12 ± 5.93to1.59 ± 5.27mL/min/1.73m2/year (p < 0.0001).Urinary protein decreased modestly without statistical significance (median0.65 - 0.55g/gCr,p = 0.155).Significant improvements in eGFR slope were observed regardless of baseline urinary protein level or the reduction rate.Multivariable analysis revealed that a reduction in serum uric acid (β = - 0.26, p < 0.001), but not urinary protein, was independently associated with theΔeGFR slope. Dapagliflozin significantly improves the eGFR slope,which was not statistically associated with urinary protein changes in this cohort, in routine clinical practice.These findings underscore the clinical value of eGFR slope-based evaluation for monitoring individualized therapeutic responses.

Aim . To summarize the available data on the effects of first-line antihypertensive agents – angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) – on serum uric acid (UA) levels in adults with (arterial hypertension) AH, with the goal of optimizing pharmacotherapy in patients with AH and asymptomatic hyperuricemia. Material and methods . A comprehensive search was conducted in PubMed, the Cochrane Central Register of Controlled Trials (CENTRAL) within the Cochrane Library, eLIBRARY, Google Scholar, and the National Institutes of Health clinical trials registry ClinicalTrials.gov. The systematic review was prepared in accordance with PRISMA guidelines. No restrictions were placed on the year of publication during the search and analysis. Results . Analysis of nine randomized controlled trials of ACEIs showed that enalapril, captopril, and fosinopril demonstrated neutrality with respect to UA levels, whereas other drugs in this class may increase UA concentrations. Analysis of eleven randomized controlled trials of ARBs showed that only losartan exhibits a uricosuric effect, while irbesartan, valsartan, and eprosartan are metabolically neutral. Conclusion . Among ACEIs, enalapril, low-dose ramipril, and fosinopril exhibit the most favorable safety profile and the greatest neutrality regarding UA levels. ARBs are generally metabolically neutral with respect to UA, with the exception of losartan, which possesses a uricosuric effect.