Search Results (163)

Background/Objectives: The acute kidney injury (AKI) to chronic kidney disease (CKD) transition has been associated with a failed-repair proximal tubule (FR-PT) cell state. Hyperuricemia is an established CKD risk factor, but whether FR-PT cells have a coordinated metabolic signature reproducibly detectable across mouse models and human kidney disease remains unresolved. Methods: We assembled a pre-registered meta-analysis of 16 public mouse-kidney metabolomic cohorts (383 samples; five model classes; three injury phases) through a three-path harmonization pipeline. Convergent validation drew on KPMP single-nucleus RNA-seq (78,480 proximal tubule cells), two-sample Mendelian randomization of serum urate (102 instruments) against AKI/CKD/eGFR GWAS, and cross-cohort human plasma metabolomics across 2058 CKD/DKD patients. Results: Mouse meta-analysis identified uric acid (g = +2.70) and AICAR (g = +1.50) as the only cross-class conserved metabolites, with uric acid peaking during the AKI-to-CKD transition and returning to baseline in mouse CKD due to uricase clearance. Cross-class overlap between model classes was low (mean pairwise Jaccard = 0.109, below the pre-registered 0.20 threshold), invoking the pre-registered M-S1 stop rule: model-specific metabolic responses dominate, and the conserved signal is a small two-metabolite core superimposed on these largely model-specific programs. KPMP failed-repair PT cells exhibited transcriptional patterns consistent with coordinated four-arm purine-pathway dysregulation (de novo synthesis ↑, AMPK ↑, MOCOS ↑, URAT1 ↓), with this transcriptional pattern observed in both AKI and CKD donors (Spearman ρ = +0.900). Mendelian randomization was consistent with a possible causal contribution of serum urate to AKI/CKD/eGFR risk, with colocalization evidence at GCKR (PP.H4 = 1.000). Cross-cohort human plasma profiling across 2058 patients confirmed the systemic detectability of 29 purine-pathway metabolites in uricase-deficient humans (a translational-plausibility check, not validation of cellular source). Conclusions: The integrated data support a model in which FR-PT-associated purine-pathway reprogramming may contribute to the elevated urate signal observed during AKI-to-CKD transition, with uric acid as the candidate metabolic readout. Differences in uricase activity between mice and humans may help explain why chronic-phase urate signals are attenuated in mice but persist in humans. This work nominates a candidate cell-state metabolic readout of the AKI-to-CKD transition as a hypothesis for prospective testing; it does not establish causation, and therapeutic translation would require dedicated interventional studies. Full article

Gout is a systemic metabolic inflammatory disease driven by hyperuricemia and monosodium urate crystal deposition, and is frequently accompanied by chronic kidney disease and uric acid nephrolithiasis. Current evidence indicates that acidic urine, hypocitraturia, and insufficient ammonium excretion are common in gout patients, and may be associated with insulin resistance, impaired renal ammoniagenesis, and abnormalities in tubular acid-base regulation. Persistent urinary acidification may contribute to the development and progression of uric acid stone formation and gout-related renal injury by reducing uric acid solubility, promoting crystal formation and intratubular deposition, and decreasing renal uric acid clearance. Urinary alkalization therapy can increase urine pH, thereby enhancing uric acid solubility and excretion, and has shown potential in some studies to improve serum urate levels, proteinuria, renal function parameters, and gout flare frequency, especially when using citrate-based alkali. However, the currently available evidence is mainly derived from observational studies and small prospective investigations, and recommendations across international guidelines remain inconsistent. High-quality evidence is still lacking regarding the optimal target population, urine pH range, choice of alkalizing agents, monitoring strategies, and long-term efficacy. Well-designed prospective studies are therefore needed to clarify the clinical role of urinary alkalization in renal protection among patients with gout. Full article

Background/Objectives: Cardiovascular risk (CVR) prediction using SCORE2 may incompletely capture the burden of subclinical atherosclerosis in patients with chronic inflammatory conditions. Identifying simple, accessible markers to refine risk stratification remains an unmet need. This study aimed to evaluate whether serum urate improves detection of subclinical atherosclerosis beyond SCORE2 in a psoriatic arthritis cohort. Methods: We conducted a cross-sectional study including 250 patients with psoriatic arthritis fulfilling CASPAR criteria. Vascular assessment comprised carotid and femoral ultrasound and abdominal radiography. Atherosclerotic plaque was defined according to Mannheim criteria. The main outcomes were global plaque (≥1 vascular territory) and extended plaque (≥2 territories). Multivariable logistic regression adjusted for SCORE2 categories assessed independent associations. Incremental value was evaluated using decision curve analysis (DCA), category-free net reclassification improvement (cfNRI), and integrated discrimination improvement (IDI). Results: Hyperuricemia prevalence was 21.6%. Patients with hyperuricemia showed a higher prevalence of global plaque (88.9% vs. 62.8%, p < 0.001). After adjustment for SCORE2, serum urate was independently associated with global plaque (OR 4.23, 95% CI 1.26–14.2). Notably, 64.3% of patients classified as low–moderate risk already exhibited plaque. In the 50–69-year subgroup, adding serum urate improved reclassification (cfNRI +0.60; IDI +0.031) and was associated with higher net clinical benefit across decision thresholds. The combined model (SCORE2+HU+cIMT) achieved the highest curves, although with limited incremental gain over HU alone. Conclusions: SCORE2 categories showed substantial discordance with imaging-defined subclinical atherosclerotic burden in this population. Serum urate, an inexpensive and widely available marker, may help refine cardiovascular risk stratification and identify patients who could benefit from further vascular assessment. Full article

Hyperuricemia (HUA) is a common immunometabolic disorder associated with gout, renal dysfunction, and systemic inflammation, yet the molecular targets through which non-starch polysaccharides (NSPs) may modulate HUA-related inflammation remain unclear. Here, we applied an integrative bioinformatics and computational workflow combining public transcriptomic datasets, curated NSP-related targets, protein–protein interaction analysis, enrichment analysis, single-cell RNA sequencing, and Mendelian randomization. We further included GutMGene-based orthogonal support analysis, guided docking, structural dynamics analysis, exploratory ADMET profiling, and in silico TLR4 knockout to extend target prioritization. This approach prioritized a TLR4-centered inflammatory module, with TLR4, MSR1, TIRAP, and CXCL8 emerging as candidate genes. Enrichment analyses linked these genes to innate immune and NF-$\kappa$B-related pathways, whereas single-cell analyses localized the prioritized signals mainly to myeloid compartments during gout flares. Mendelian randomization suggested positive associations between genetically predicted expression of TLR4-axis genes and serum uric acid levels. Under electrostatic-guided docking conditions, fucoidan and alginate yielded plausible interaction models with TLR4, and normal mode and RMSF analyses suggested altered flexibility in the MD-2 region. In silico Tlr4 knockout further perturbed urate-handling programs in renal proximal tubule-enriched cells. Together, these findings do not establish TLR4 as a newly discovered hyperuricemia gene or confirm direct receptor antagonism by NSPs, but they provide an NSP-oriented integrative framework that prioritizes the TLR4 axis, highlights myeloid-cell relevance, and nominates fucoidan and alginate for experimental follow-up. Full article

Background/Objectives: Hyperuricemia may influence cognitive function, but current evidence remains inconsistent. This study examined the association between hyperuricemia/gout and cognitive impairment through a prospective cohort study and a systematic review of cohort studies. Methods: Data from 1959 Taiwan Biobank participants aged ≥60 years without mild cognitive impairment (MCI) or dementia at baseline were analyzed over a mean follow-up duration of 4.47 years (2012–2021). Cognitive function was assessed using the Mini-Mental State Examination (MMSE). Participants were classified by changes in serum uric acid status from baseline to follow-up, and Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). For the systematic review, cohort studies published up to March 2026 were identified from eight databases. Results: During follow-up, 1013 participants developed incident MCI and 132 developed dementia. Compared with participants who maintained normal serum uric acid levels, those who developed hyperuricemia during follow-up had a significantly lower MCI risk (HR = 0.72, 95% CI = 0.57–0.90), as did those with persistent hyperuricemia (HR = 0.78, 95% CI = 0.64–0.95). No significant association was observed for dementia. The systematic review of five prospective cohort studies comprising 2,261,704 participants showed inconsistent findings with considerable heterogeneity (I² = 96.7%). Conclusions: Rising serum uric acid levels were associated with lower MCI risk, but not dementia. These findings should not be interpreted as support for intentionally increasing serum uric acid levels or withholding urate-lowering therapy. Further long-term studies are needed. Full article

Per- and polyfluoroalkyl substances (PFAS) are persistent chemicals with substantial bioaccumulation potential, but their distribution between blood and urine in humans remains poorly characterized. In this review, we assessed the urine-to-blood concentration ratio (UtBCR) as a potential indicator of PFAS bioaccumulation by integrating evidence from human biomonitoring studies and protein-binding data. We summarized PFAS concentrations in human serum and urine across general and highly exposed populations and identified clear compound-specific differences in blood–urine partitioning. We further examined the associations of UtBCR with carbon chain length, biological half-life, and binding-related parameters for human serum albumin (HSA), liver fatty acid-binding protein (L-FABP), and several renal transporters. Pairwise correlation analysis and partial least squares regression indicated that UtBCR was closely associated with major toxicokinetic determinants, particularly protein-binding affinity, carbon chain length, and biological half-life. Parameters related to FABP, HSA, urate transporter 1 (URAT1), and organic anion transporter 4 (OAT4) showed more consistent associations with UtBCR than those related to organic anion transporters 1(OAT1) and organic anion transporter 3 (OAT3), suggesting that plasma/tissue binding and tubular reabsorption may contribute more than active tubular secretion to PFAS blood–urine partitioning. Overall, UtBCR appears to be a useful toxicokinetic metric for comparing the relative bioaccumulation potential of PFAS. Full article

Background/Objectives: Chronic urate nephropathy (CUN), also referred to as gouty nephropathy, represents a severe renal disease primarily precipitated by long-term hyperuricemia (HUA) and gout. However, the precise molecular mechanisms underlying its pathogenesis remain poorly understood. The present study was designed to explore these mechanisms from the perspective of targeted metabolomics. Methods: The HUA mice constructed by urate oxidase (Uox) gene knockout (KO) and their corresponding wild-type controls were employed for the present study. Serum clinical biochemical parameters were determined, and renal histopathological changes were evaluated using hematoxylin-eosin (HE) staining and Masson’s trichrome staining. A targeted metabolomic strategy based on multiple reaction monitoring (MRM) was utilized to profile the renal metabolic landscape of Uox-KO mice, and potential metabolic biomarkers for CUN were identified via multivariate data analysis. Results: Clinical biochemical analysis revealed a significant elevation in serum uric acid, creatinine, and urea nitrogen levels in Uox-KO mice compared with control mice. Histopathological observations confirmed a typical CUN phenotype in Uox-KO mice, characterized by renal tubular vacuolar degeneration and dilatation, desquamation of tubular epithelial cells into the lumen, neutrophil infiltration, glomerular crowding, and renal interstitial fibrosis. Metabolomic analysis identified a total of 291 differentially regulated metabolites in Uox-KO mice relative to control animals. These perturbed metabolites were involved in multiple key biochemical pathways, including amino acid biosynthesis, ABC transporter signaling pathway, purine metabolism, aminoacyl-tRNA biosynthesis, protein digestion and absorption, glycerophospholipid metabolism, and serotonergic synaptic transmission. Notably, pathological parameters, including biochemical measurements and histological observations, were significantly correlated with key differential metabolites associated with CUN progression. Furthermore, eleven differential metabolites (pyroglutamic acid, fructose, riboflavin, dimethyl-L-arginine, glucaric acid, indoxyl sulfate, palmitoylethanolamide, trimethylamine N-oxide, 3-hydroxyanthranilic acid, spermidine, and hippuric acid) were identified as potential metabolic biomarkers for the diagnosis and prognosis of CUN. Conclusions: These findings illustrate that targeted tissue metabolomic analysis constitutes a powerful tool for deciphering the molecular mechanisms of diseases, thus offering novel insights into the pathogenesis of CUN. Full article

This study aimed to optimize the ultrasonic-assisted extraction of polyphenols from Archidendron clypearia and to evaluate their anti-hyperuricemic effects. Polyphenols from medicinal plants have attracted increasing attention due to their potential roles in regulating uric acid metabolism. In this study, single-factor experiments combined with Box–Behnken response surface methodology were employed to optimize extraction conditions, and an entropy weighting method was applied to integrate total polyphenols and Archidendrin I into a comprehensive evaluation index. The bioactivity of the obtained extract was further assessed through in vitro assays and a hyperuricemic mouse model. The optimal extraction conditions were determined to be 50% ethanol, a liquid-to-material ratio of 30, and 31 min of sonication, yielding 175 mg GAE/g DW of total polyphenols and 80.34 mg/g DW of Archidendrin I. The extract exhibited significant xanthine oxidase inhibitory activity, reduced serum uric acid levels, regulated urate transporters (URAT1, GLUT9, and ABCG2), and alleviated renal and hepatic injury in hyperuricemic mice. These findings indicate that the optimized process enables efficient extraction of polyphenols from Archidendron clypearia, and the resulting extract exerts beneficial regulatory effects on uric acid metabolism, highlighting its potential as a natural agent for hyperuricemia management. Full article

Hyperuricemia, a common metabolic disorder characterized by elevated serum uric acid (UA) levels, can lead to severe complications such as gout and renal impairment. Conventional therapies, while effective, are frequently accompanied by significant adverse effects, underscoring the urgent need for safer therapeutic alternatives. Recent evidence identifies the intestine as a novel, pivotal regulator of UA homeostasis, presenting a promising therapeutic axis. This review delineates the intestinal mechanisms governing UA regulation and evaluates the therapeutic potential of natural active substances that target these pathways. We conducted a comprehensive review of recent preclinical studies focusing on intestinal mechanisms involved in UA metabolism, including the roles of gut microbiota, urate transport proteins, intestinal barrier function, and inflammation. Studies evaluating natural active substances—such as polyphenols, polysaccharides, peptides, and plant extracts—were systematically analyzed for their effects on gut-mediated UA regulation. Natural active substances have been shown to effectively alleviate hyperuricemia by modulating gut microbiota, enhancing UA intestinal excretion, reinforcing intestinal barrier function, and suppressing inflammatory pathways. Collectively, these findings demonstrate the multi-target efficacy of natural active substances within the intestines, offering a promising therapeutic strategy that warrants further investigation into nutrition-based intestinal interventions and novel pharmacological treatments for hyperuricemia. Full article

Background: Hyperuricemia (HUA) is a metabolic disorder that severely threatens human health. Chronic uric acid (UA) overload promotes the progression of tubulointerstitial fibrosis (TIF), leading to impaired UA excretion. Our previous studies identified HIPK2 inhibitor XRF-1021, which exhibits robust anti-TIF activity and lowers UA levels in vivo. This study aimed to elucidate its UA-lowering mechanism and therapeutic potential for HUA. Methods: Uricase and xanthine oxidase (XOD) assays were performed to assess effects on UA degradation/production. HEK293T cells transiently expressing UA transporters and gene-knockdown rats were used to evaluate transporter inhibition, while HK-2 cells were analyzed by Western blot. Pharmacokinetics were characterized in rats. Efficacy was tested in potassium oxonate-induced acute HUA rats, diet/adenine-induced chronic HUA quails, and adenine-induced mice with HUA secondary to TIF. Maximum tolerated dose and long-term toxicity were assessed in rats. Results: XRF-1021 neither activated uricase nor inhibited XOD, indicating no direct effect on UA catabolism or synthesis. Instead, XRF-1021 inhibited URAT1 and GLUT9, reducing renal UA reabsorption, while sparing OAT3, OAT4, and ABCG2 activity and upregulating OAT3 and NPT4, suggesting minimal risk of disrupting drug or uremic toxin handling. XRF-1021 showed dose-dependent systemic exposure in rats, lowered serum UA, and provided renal protection in vivo. LD₅₀ values were 2345.4 mg/kg (male) and 1078.9 mg/kg (female), with no obvious toxicity after long-term dosing. Conclusions: XRF-1021 lowers UA by inhibiting URAT1 and GLUT9 to enhance renal UA excretion and provides kidney protection, supporting XRF-1021 as a promising candidate for HUA therapy. Full article

Hyperuricemia is a metabolic disorder characterized by elevated serum uric acid levels and is increasingly linked to alterations in intestinal mucosal condition and gut microbiota composition. Probiotics have been proposed as safe, non-pharmacological approaches for managing hyperuricemia, but strain-specific evidence remains limited. This study aimed to evaluate the anti-hyperuricemic potential of Limosilactobacillus reuteri MBHC10138, isolated from human breast milk, and to examine its association with purine metabolism–related parameters, renal morphological features, intestinal barrier-associated markers, and gut microbiota composition. In vitro, MBHC10138 effectively degraded purine nucleosides that are metabolized into uric acid, suggesting its potential to reduce uric acid production in the host. In a mouse model of diet- and oxonate-induced hyperuricemia, oral administration of MBHC10138 significantly lowered serum uric acid levels to a level comparable with allopurinol treatment, while improving renal morphology. Histological and molecular analyses demonstrated restoration of the tight junction proteins zonula occludens-1 and occludin, indicative of enhanced intestinal barrier integrity. Furthermore, MBHC10138 administration modulated the gut microbiota by restoring microbial α-diversity and significantly increasing the relative abundances of the Clostridia vadinBB60 group and Oscillospiraceae, taxa associated with butyrate production, compared with the allopurinol-treated group. Collectively, these findings indicate that MBHC10138 exerts dual actions against hyperuricemia and intestinal barrier dysfunction through the regulation of purine metabolism, promotion of renal urate excretion, and modulation of gut microbial composition. MBHC10138 may thus represent a promising probiotic candidate for the prevention and adjunctive management of hyperuricemia-related metabolic disorders. Full article

Background/Objectives: Hyperuricemia (HUA) is the second most common metabolic disease in China (24.5% in males, 3.6% in females), which can induce multiple complications such as gout and diabetes. Existing urate-lowering drugs have significant hepatorenal toxicity, necessitating safe lifestyle interventions. Electrolyzed alkaline water (EAW) as daily drinking water has shown preliminary effectiveness, but it lacks randomized controlled evidence and mechanistic studies at the microbiome–metabolome interface. Methods: We conducted a 12-week randomized controlled trial in 40 adults aged 18–65 years with elevated serum uric acid (SUA). Participants consumed either 1.5 L/day of EAW (pH 8.5–9.5) or purified water (pH 7.0). Clinical indicators, quality of life (SF-36), gut microbiota, and gut metabolomics were comprehensively assessed to evaluate intervention efficacy and explore potential mechanisms. Results: After 12 weeks, the EAW group exhibited a larger reduction in serum uric acid than the control group, along with improvements in selected physical health-related quality-of-life measures. Modest differences in gut microbial composition were observed between groups. Metabolomic analyses identified group-level differences in metabolites enriched in pathways related to purine metabolism and other urate-associated metabolic processes. Conclusions: This pilot randomized controlled trial suggests that consumption of EAW is associated with a modest reduction in serum uric acid. Exploratory multi-omics analyses indicate concurrent changes in gut microbiota and metabolic profiles. These findings support further investigation of electrolyzed alkaline water as a potential adjunctive, non-pharmacological option for hyperuricemia in larger and longer-term studies. Ethics: This trial was registered with the Chinese Clinical Trial Registry under the identifier ChiCTR2500100190. Ethical approval for the present study was granted by the Nankai University Institutional Review Board (NKUIRB2025001, 23 January 2025). Full article

Background: d-Limonene (LIM) is a food-derived monoterpenoid phytocompound predominantly found in citrus peels, endowed with potent antioxidant and anti-inflammatory properties, and has been reported to inhibit xanthine oxidase (XO) activity in vitro. This study investigated the dose-sparing efficacy of this dietary bioactive compound in combination with low-dose allopurinol (ALP) using a dual rat model combining potassium oxonate (PO)-induced hyperuricemia and monosodium urate (MSU)-triggered gouty arthritis, thereby capturing both metabolic and inflammatory dimensions of gout. Methods: Female Wistar rats were PO-primed and MSU-challenged, then treated with LIM (50 mg/kg), ALP (5 or 10 mg/kg), or LIM + ALP. Outcomes included paw thickness, dysfunction and inflammation indices, serum uric acid, urea, creatinine, AST/ALT, cytokines (IL-1β, TNF-α, IL-6), oxidative stress markers (MDA, SOD, catalase, GSH), and NLRP3 immunoreactivity, supported by radiographic and histopathological analyses. Data were analyzed by one-way ANOVA with Tukey’s post hoc test. Results: LIM improved clinical and biochemical outcomes versus monotherapies. However, LIM + low-dose ALP exhibited the greatest overall efficacy. On Day 30, paw thickness was significantly lower with LIM + ALP than with LIM alone (3.25 ± 0.31 vs. 3.98 ± 0.72 mm; p < 0.001). Serum uric acid and hepatic transaminases declined most with the combination (p < 0.0001 vs. LIM), accompanied by improved renal indices (p < 0.001). Pro-inflammatory cytokines were markedly reduced, NLRP3 immunostaining was minimal, and oxidative balance shifted toward homeostasis (↓ MDA; ↑ SOD, catalase, GSH). Radiographic and histological evaluations corroborated attenuation of joint inflammation and tissue damage. Conclusions: In the PO + MSU gout model, co-administration of the food-derived compound LIM with low-dose ALP achieved additive, dose-sparing benefits across metabolic, inflammatory, and histological endpoints. While in vivo XO activity was not directly assessed, the findings are consistent with XO-pathway modulation, NLRP3–IL-1β suppression, and redox restoration. These results highlight the potential of dietary bioactives such as d-Limonene to complement standard urate-lowering therapy, warranting further pharmacokinetic and safety validation. Full article

The acute gouty arthritis (AGA) to chronic gouty arthritis (CGA) transition is a critical phase leading to irreversible joint damage and systemic complications. However, current molecular mechanism investigations have remained limited to single-omics approaches that lack comprehensive multi-omics explorations. We integrate high-depth data-independent acquisition (DIA) proteomics and untargeted metabolomics to analyze serum samples from healthy controls (n =28), AGA (n = 31), and CGA (n = 14) patients to address this gap. Through differential expression analysis, we identified nine persistently dysregulated pivotal proteins with robust discriminative capacity, including the urate excretion regulator ZBTB20 and inflammation/immune-related proteins (GUCY1A2, CNDP1, LYZ, SERPINA5, GSN). Additionally, 11 consistently altered core metabolites with diagnostic potential were detected, indicating perturbations in sex hormones, thyroid hormones, gut microbiota-derived metabolites, environmental exposures, and nutritional factors. Multi-omics KEGG enrichment analysis highlighted thyroid hormone synthesis, AMPK signaling pathway, and taurine and hypotaurine metabolism as central pathways. Correlation network analysis further revealed significant immune dysregulation, illustrating an evolution from acute immune activation to chronic inflammation during AGA-to-CGA progression. Our study establishes that a coordinated disruption of the thyroid hormone–AMPK–taurine metabolic axis and concomitant immune microenvironment remodeling is associated with chronic gout development. These findings provide critical targets for developing early diagnostic indicators and targeted interventions for CGA. Full article

Background and Objectives: Cardiometabolic diseases are rising in Latin America, yet rural Amazonian populations remain understudied. We aimed to characterize the prevalence and factors associated with a simple composite cardiometabolic risk in rural Amazonian adults. Materials and Methods: We conducted an analytical cross-sectional study during community screenings in San Martín, Peru, in 2025, enrolling adults aged ≥ 18 years. The outcome was present when ≥2 biological/anthropometric alterations were identified at the same visit (hypertension, dyslipidemia, hyperglycemia, hyperuricemia, general obesity, abdominal obesity, or elevated waist-to-hip ratio). Behaviors included current tobacco use, alcohol risk (AUDIT), and physical activity (IPAQ). We summarized variables (univariate), compared groups (bivariate: chi-square; Fisher for alcohol), and fitted modified Poisson regression with robust errors to estimate prevalence ratios (PRs); variables with p ≤ 0.20 in bivariate analysis entered multivariable models. Results: We enrolled 205 adults; 70.2% met the composite outcome. In multivariable models, abdominal obesity (adjusted PR [aPR] 1.70; 95% CI 1.40–2.10), hyperglycemia (1.65; 1.25–2.17), hyperuricemia (1.38; 1.19–1.61), dyslipidemia (1.25; 1.07–1.46), and general obesity (1.21; 1.04–1.40) were independently associated with cardiometabolic risk. Hypertension (1.06; 0.88–1.29) and elevated waist-to-hip ratio (1.20; 0.88–1.63) were not. Physical activity differed crudely but showed no independent association; tobacco and alcohol were not associated. Conclusions: In this rural Amazonian population, we observed a high prevalence of composite cardiometabolic risk and found that central adiposity and metabolic derangements, not blood pressure or self-reported behaviors, were the main correlates. Simple measures such as waist circumference, fasting glucose or HbA1c, a basic lipid panel, and serum urate may help flag adults at higher cardiometabolic risk in similar low-resource primary-care settings, but prospective studies are needed to evaluate their predictive value and screening performance. Full article