OBJECTIVE:To systematically evaluate the contribution of clinical heterogeneity to chronic kidney disease (CKD) progression in gout patients using data-driven phenotyping, and to assess whether incorporating genetic risk improves prediction of renal outcomes. METHODS:In this prospective cohort study, 1497 Chinese gout patients were enrolled and followed for CKD progression. K-means clustering was applied to four core clinical variables: serum urate (SU), fractional excretion of uric acid (FEUA) (i.e. high- and low-excretion), gout duration and kidney stone burden. The primary outcome was the incidence of CKD stage ≥3, assessed using Cox proportional hazards models. Genetic risk was evaluated using an unweighted genetic risk score derived from 20 single nucleotide polymorphisms associated with gout and hyperuricaemia. RESULTS:Over a follow-up of 4166 person-years, 153 participants (10.22%) developed CKD stage ≥3. Five clinical clusters were identified: Cluster 1 (high-excretion, low-urate), Cluster 2 (low-excretion, low-urate), Cluster 3 (long-duration), Cluster 4 (low-excretion, high-urate) and Cluster 5 (nephrolithiasis). Cluster 4 and Cluster 5 were significantly associated with increased risk of CKD progression, with adjusted hazard ratios of 2.19 (95% CI 1.20-4.01) and 3.52 (95% CI 1.91-6.48), respectively. Genetic predisposition, via risk score, further amplified renal risk in Cluster 4. Achieving target SU levels and reductions in kidney stone burden were independently associated with a lower risk of CKD progression. CONCLUSIONS:This study proposes a novel K-means clustering-based classification of gout, identifying subgroups with distinct CKD trajectories. Integration of clinical phenotyping and genetic profiling may enhance individualized risk stratification and guide targeted prevention strategies in gout-associated CKD.

BACKGROUND:Activated charcoal (AC), a known adsorbent in the gastrointestinal tract, has been reported to reduce serum urate (SU) levels. This study aimed to assess the efficacy and safety of AC in managing primary gout. METHODS:This double-blind, double-dummy, randomized controlled trial involved 348 patients, who were randomly assigned to one of four groups: febuxostat 40 mg, febuxostat 20 mg + AC 4.5 g, febuxostat 20 mg + AC 7.2 g, and febuxostat 20 mg. Patients were followed-up every 4 weeks until week 24. The primary endpoint was the proportion of patients achieving SU level < 360 μmol/L. RESULTS:All 348 enrolled patients were included in analysis. The febuxostat-AC combination regimen didn't demonstrate superior efficacy in controlling SU levels. However, the combination regimen significantly reduced flare rates compared to the febuxostat 20 mg group (≥ 1 and ≥ 3 flares, P < 0.05) and the febuxostat 40 mg group (≥ 1 flare, P < 0.05; ≥ 3 flares, P < 0.01), and it also significantly prolonged the time to first flare. Additionally, the combination regimen resulted in significantly lower low-density lipoprotein cholesterol (LDL-C) levels at week 24. The incidence of adverse events was similar across the groups. CONCLUSIONS:The febuxostat-AC combination regimen didn't enhance urate-lowering effects but significantly reduced gout flare frequency, delayed the onset of first flare, and improved LDL-C levels. These findings underscore the role of AC in comprehensive gout management. TRIAL REGISTRATION:ChiCTR, http://www.chictr.org.cn, ChiCTR2000034138.

People with gout and combined-type hyperuricemia, defined as renal urate overload and renal urate under-excretion, have diminished responsiveness to urate-lowering therapy. Emerging observational data suggest that urine alkalization might improve responsiveness to febuxostat. Hence, this prospective study evaluated the urate-lowering efficacy of citrate mixture added to febuxostat in people with gout and combined-type hyperuricemia. Patients with combined-type hyperuricemia and low urine pH (< 6.2) were prospectively enrolled from a gout clinic. All were treated with febuxostat (initially 20 mg daily, escalated to 40 mg daily if serum urate (SU) ≥360µmol/L). Citrate mixture (3.5 g twice daily, open label) was added according to shared decision of both physician and patient (alkalization vs. non-alkalization). Participants were followed for 12 weeks, with primary endpoint being achievement of SU < 360 µmol/L at final assessment. We enrolled 234 eligible patients, with 194 completing 12 weeks follow-up (98 non-alkalization and 96 with alkalization). At week 12, more patients in the alkalization group achieved SU < 360µmol/L (57.3

Purpose:To evaluate the effect of urine alkalization with citrate mixture on reducing flare incidence during initial urate-lowering therapy period in male gout patients with renal underexcretion-type. Patients and Methods:In this prospective cohort study, patients with renal underexcretion and urinary pH < 6.2 were enrolled. All participants received febuxostat 20 mg/day during weeks 0-4, later increased to 40 mg/day if serum urate (SU) levels > 360 μmol/L. According to group assignment, patients received either alkalization therapy (Alk group; citrate mixture, 3.5 g twice/day) or no alkalization (Control group). The primary outcome measure was gout flare incidence. Results:In total, 240 patients (Alk 114, Control 126) completed the 12-week follow-up. The Alk group had a significantly lower flare incidence (35.1%) than the Control group (59.5%, P < 0.001) and a lower recurrence of flares (14.0% vs. 31.0%, P = 0.002). At week 4, the proportion of participants with SU < 360 μmol/L was significantly higher in the Alk than in the Control group (P = 0.039). The Alk group had lower triglycerides and higher high-density lipoprotein cholesterol levels than the Control group at weeks 4, 8, and 12 (P < 0.05). The urinary albumin-to-creatinine ratio (UACR) decreased from 1.65 (0.36-7.01) to 1.08 (0.62-2.99) at week 12 in the Alk group, significantly lower than that in the Control group (P = 0.001). No significant difference was noted in the incidence of adverse events between groups. Conclusion:In patients with renal underexcretion gout, urine alkalization with febuxostat therapy prevented gout flares, improved lipid metabolism, and lowered UACR. Study Registration:ChiCTR, https://www.chictr.org.cn, ChiCTR2100043573.

BACKGROUND:In 2018, the Chinese Society of Endocrinology developed the "Chinese guideline for diagnosis and treatment of hyperuricemia and gout (2019)". Over the past 5 years, clinical and experimental research has expanded our knowledge of gout, resulting in novel diagnostic and therapeutic approaches. This update, prompted by new clinical challenges and gaps in evidence, aims to refine the 2019 guidelines. METHODS:The working group formulated clinical questions based on a nationwide questionnaire survey, and the expert panel evaluated new evidence addressing these questions from January 2019 to March 2025. The guideline development followed the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach, adhering to internationally recognized protocols for clinical practice guideline development. RESULTS:The update includes 26 recommendations addressing 10 clinical questions related to urate-lowering therapy (ULT) for asymptomatic hyperuricemia and reproductive populations, anti-inflammatory treatments, urine alkalinization, dietary advice, and gout diagnosis in patients without a record of hyperuricemia and gout flare predictions in patients with asymptomatic hyperuricemia and intermittent gout. It recommends febuxostat as a first-line ULT for asymptomatic hyperuricemia and using it with caution during pregnancy and lactation. ULT should be customized according to the pathophysiologic type of hyperuricemia. Chronic gout management includes maintaining serum urate levels between 180 and 300 μmol/L and prolonged glucocorticoid tapering in combination with colchicine. Alkalinization with citrate is preferred over sodium bicarbonate for patients with urine pH < 6.0. Novel biomarkers for predicting gout flares are proposed for high-risk populations. CONCLUSIONS:These updated guidelines incorporate expert consensus and evidence to provide refined strategies for the diagnosis, prevention, and treatment of hyperuricemia and gout.

OBJECTIVE:This study explores alterations in renal cortical perfusion post-Early Goal-Directed Therapy (EGDT) in sepsis patients, to investigate its association with major adverse kidney events within 30 days (MAKE-30) and identify hemodynamic factors associated with renal cortical perfusion. METHODS:Sepsis patients admitted to the ICU from Jan 2022 to Jul 2023 were prospectively enrolled. Contrast-enhanced ultrasound (CEUS) assessed renal cortical perfusion post-EGDT. Hemodynamic parameters and renal resistive index (RRI) were collected. Patients were categorized into MAKE-30 and non-MAKE-30 groups. The study examined the association between renal cortical perfusion and MAKE-30, explored the hemodynamic factors related to renal cortical perfusion. RESULTS:Of 94 sepsis patients, 46 (48.9 %) experienced MAKE-30. Distinctions in pulmonary (P = 0.012) and abdominal infection sites (P = 0.001) and significant SOFA (P < 0.001) and APACHE II scores (P = 0.003) differences were observed. No significant differences in baseline characteristics, vasopressor, or diuretic doses were noted (P > 0.05). Hemodynamic parameters in MAKE-30 and non-MAKE-30 patients showed no significant differences. RRI was higher in MAKE-30 patients (0.71 vs 0.66 P = 0.005). Renal microcirculation parameters, including AUC (p = 0.035), rBV (p = 0.021), and PI (p = 0.003), were lower in MAKE-30. Reduced cortical renal perfusion was associated with an increased risk of MAKE-30. Renal cortical perfusion RT was identified as an independent factor associated with this risk (HR 2.278, 95 % CI (1.152-4.507), P = 0.018). RRI correlated with renal cortical perfusion AUC (r = -0.220 p 0.033). CONCLUSION:Despite normal systemic hemodynamics post-sepsis EGDT, MAKE-30 patients show reduced renal cortical perfusion. CEUS-derived RT is an independent factor associated with this change. RRI correlates with renal cortical perfusion.

Objective Gout in young people is increasingly common across the world, including in China. This study aimed to identify clinical and genetic associations with early-onset gout in Chinese men. Methods One thousand two hundred and one Chinese men with gout were included. Early-onset gout was defined as the first presentation of gout at <30years. Twenty single nucleotide polymorphisms (SNPs) identified as gout-risk loci or associated with serum urate (SU) levels in East Asian populations were genotyped. Logistic regression was used to evaluate the association of SNPs and clinical factors with early-onset gout. Results Four hundred and thirty-three (36.1%) participants were identified as having early-onset gout. These patients had higher SU levels and were more likely to experience gout flares than those with later-onset gout. The ALDH2 rs671 GG genotype was associated with a lower risk of early-onset gout. Compared to those with GG genotype who never drank alcohol before gout onset, individuals with AA or AG genotypes who drank alcohol before gout onset had a higher likelihood of early-onset gout. Additionally, alcohol intake significantly increased the likelihood of gout flares in early-onset gout patients. Moreover, body mass index, sugar-sweetened beverage intake, family history of gout and renal urate underexcretion were associated with early-onset gout. Conclusions The ALDH2 rs671 GG genotype was significantly associated with a lower risk of early-onset gout, while individuals with the AA or AG genotype who consumed alcohol were more susceptible. These findings indicate that alcohol intake is a potentially modifiable risk factor for early-onset gout in genetically susceptible individuals.

OBJECTIVES:Stage ≥3 chronic kidney disease (CKD) affects ∼25% of people with gout. The effects of urate-lowering therapy (ULT) on CKD incidence and progression have remained inconclusive. Here, we assessed the impact of a gout ULT clinic intervention using artificial intelligence (AI) on CKD incidence and achievement of serum urate (SU) target. METHODS:An observational study compared propensity score (PS)-matched gout cohorts from an AI-based Gout Intelligent Management System (GIMS) and a standard Electronic Medical Records system (EMRS) clinic database. The GIMS included a mobile application, data fusion interface and modules for expert consultation and laboratory results management. All patients had gout and a starting estimated glomerular filtration rate >60 ml/min. Using a 1:2 PS-matched cohort study design, we assessed the impact of the AI-based system on CKD outcomes and ULT effectiveness over 4 years of follow-up. RESULTS:Compared with EMRS, GIMS was associated with reduced incidence of CKD stage ≥3. Specifically, 169/4117 new-onset CKD stage ≥3 (incidence 4.1 per 100 person-years) with GIMS compared with 164/2128 with EMRS (incidence 7.7 per 100 person-years) during follow-up. More participants achieved SU <6.0 mg/dl with GIMS versus EMRS during follow-up (49.8% vs 25.9%, P < 0.001). CONCLUSION:Application of the artificial intelligence-based Gout Intelligent Management System was associated with lower incidence of chronic kidney disease stage ≥3 and superior target serum urate achievement in people with gout. The Gout Intelligent Management System represents a novel approach to improve real-world renal outcomes and urate-lowering therapy success in gout.

OBJECTIVES:Gout patients frequently have decreased urine pH, related to metabolic syndrome (MetS) and chronic kidney disease. Here, we aimed to investigate whether the addition of urine alkalization to urate-lowering therapy (ULT) is associated with improvements in albuminuria, gout flares or MetS outcomes in men with gout and low urinary pH (pH < 6.2). METHODS:A prospective cohort study enrolled 385 participants starting ULT with febuxostat (initially 20 mg daily, escalated to 40 mg daily if serum urate ≥360 µmol/l), with or without alkalization based on patient preference using a 3.5 g bid citrate mixture. Participants were followed every 4 weeks to week 12. The primary outcome was urine albumin-to-creatinine ratio (UACR) at week 12. RESULTS:In total, 343 participants completed the week 12 visit (137 alkalization, 206 controls). At week 12, compared with controls, participants receiving alkalization required a significantly lower febuxostat dose (by ∼20%) but had no significant difference in serum urate at target <360 µmol/l. Urine pH increased significantly in the alkalization group from week 4 (P < 0.001). At week 12, the alkalization group had a significantly lower UACR compared with control (P < 0.001), without significantly different eGFR. Participants in the alkalization group experienced fewer gout flares and had lower pain visual analogue scale scores (P < 0.001). There were lower serum triglyceride levels (P < 0.01) and higher HDL-C levels (P < 0.001) in the alkalization group. No other differences in metabolic outcomes were observed. CONCLUSION:Urine alkalization was associated with lower UACR, fewer gout flares, and improved serum lipid profile in febuxostat-treated men with gout and low urine pH. TRIAL REGISTRATION:ChiCTR, http://www.chictr.org.cn, ChiCTR2100043573.

OBJECTIVES:To identify specific metabolomic profiles associated with gout flares in people with gout. METHODS:Participants with gout were sequentially enrolled. In cross-sectional analysis, data were analysed according to the presence of gout flare (acute group) or absence of gout flare (intercritical group) at the time of enrolment. Participants in the intercritical group were prospectively followed and analysed according to the development of gout flares (recurrent flare group) or no gout flare (no flare group) over 1 year. Relative abundances of metabolites in serum obtained at the baseline visit were measured by untargeted liquid chromatography-mass spectrometry. Risk of incident flare was analysed using least absolute shrinkage and selection operator (LASSO)-Cox regression and time-receiver operating characteristic (ROC). Machine learning models were performed to identify biomarkers in cross-sectional and longitudinal analysis, which was further optimised using quantitative targeted metabolomics in an independent validation cohort. RESULTS:Participants in the acute and intercritical groups showed distinct metabolic profiles, including carbohydrate, lipid and nucleotide metabolism. Many metabolites were associated with recurrent gout flare in the prospective analysis. The metabolic risk score with six LASSO-derived metabolites, including 5-methoxytryptamine, differentiated well for gout flare risk, yielding an area under the ROC curve (AUC) of 0.82 (95% CI 0.74 to 0.90). Machine learning models achieved an AUC of 0.828 for comparison between the acute and intercritical groups. For the prediction of recurrent flare, AUC reached 0.807-0.867 with combined metabolites and clinical measurements. CONCLUSIONS:Metabolic reprogramming differentiates between the acute and intercritical stages of gout, and implicated metabolites may serve as biomarkers for future gout flares.

OBJECTIVE:The aim of this updated guideline is to provide comprehensive recommendations for the management of gout in patients with common comorbidities, such as chronic kidney disease (CKD), cardiovascular disease (CVD), diabetes, osteoarthritis (OA), and gastrointestinal disorders. METHODS:This guideline was developed by a multidisciplinary expert panel consisting of specialists in endocrinology, rheumatology, nephrology, cardiology, gastroenterology, and methodology. The development process adhered to standard methodologies, including PICO (population, intervention, comparator, and outcomes) question deconstruction, systematic literature review, the Grading of Recommendations Assessment, Development and Evaluation (GRADE) for evidence and recommendation evaluation, Delphi voting, and expert consensus. RESULTS:The guideline presents 26 evidence-based recommendations addressing seven clinical questions for patients with hyperuricemia and gout in the context of comorbidities. Key recommendations include the maintenance of strict serum urate targets, particularly for patients with CKD stage ≥ 3, chronic gouty arthritis, and OA, in order to prevent disease progression. In patients with CVD or diabetes, intra-articular triamcinolone is preferred over systemic glucocorticoids. Prioritized anti-inflammatory treatments for patients with CKD, gastrointestinal diseases, and OA are recommended. The guideline also introduces emerging therapies, such as interleukin-1 inhibitors and selective urate transport inhibitors, as potential treatment options for refractory cases. CONCLUSION:The update offers a comprehensive, patient-centered approach to managing gout, particularly in individuals with associated comorbidities. Multidisciplinary collaboration and emerging new treatments and evidence ensure the optimization of the recommendations.

OBJECTIVE:Mechanisms underlying the adolescent-onset and early-onset gout are unclear. This study aimed to discover variants associated with early-onset gout. METHODS:We conducted whole-genome sequencing in a discovery adolescent-onset gout cohort of 905 individuals (gout onset 12 to 19 years) to discover common and low-frequency single-nucleotide variants (SNVs) associated with gout. Candidate common SNVs were genotyped in an early-onset gout cohort of 2,834 individuals (gout onset ≤30 years old), and meta-analysis was performed with the discovery and replication cohorts to identify loci associated with early-onset gout. Transcriptome and epigenomic analyses, quantitative real-time polymerase chain reaction and RNA sequencing in human peripheral blood leukocytes, and knock-down experiments in human THP-1 macrophage cells investigated the regulation and function of candidate gene RCOR1. RESULTS:In addition to ABCG2, a urate transporter previously linked to pediatric-onset and early-onset gout, we identified two novel loci (Pmeta < 5.0 × 10-8): rs12887440 (RCOR1) and rs35213808 (FSTL5-MIR4454). Additionally, we found associations at ABCG2 and SLC22A12 that were driven by low-frequency SNVs. SNVs in RCOR1 were linked to elevated blood leukocyte messenger RNA levels. THP-1 macrophage culture studies revealed the potential of decreased RCOR1 to suppress gouty inflammation. CONCLUSION:This is the first comprehensive genetic characterization of adolescent-onset gout. The identified risk loci of early-onset gout mediate inflammatory responsiveness to crystals that could mediate gouty arthritis. This study will contribute to risk prediction and therapeutic interventions to prevent adolescent-onset gout.

Urate oxidase (Uox)-deficient mice could be an optimal animal model to study hyperuricemia and associated disorders. We develop a liver-specific conditional knockout Uox-deficient (Uox CKO) mouse using the Cre/loxP gene targeting system. These Uox CKO mice spontaneously developed hyperuricemia with accumulated serum urate metabolites. Blocking urate degradation, the Uox CKO mice showed significant de novo purine biosynthesis (DNPB) in the liver along with amidophosphoribosyltransferase (Ppat). Pegloticase and allopurinol reversed the elevated serum urate (SU) levels in Uox CKO mice and suppressed the Ppat up-regulation. Although urate nephropathy occurred in 30-week-old Uox CKO mice, 90 % of Uox-deficient mice had a normal lifespan without pronounced urate transport abnormality. Thus, Uox CKO mice are a stable model of human hyperuricemia. Activated DNPB in the Uox CKO mice provides new insights into hyperuricemia, suggesting increased SU influences purine synthesis.

OBJECTIVE:Hyperuricemia can be stratified into four subtypes according to renal uric acid handling. The aim of this study was to comprehensively describe the biologic characteristics (including genetic background) of clinically defined hyperuricemia subtypes in two large geographically independent gout cohorts. METHODS:Hyperuricemia subtype was defined as renal uric acid overload (ROL), renal uric acid underexcretion (RUE), combined, or renal normal. Twenty single nucleotide polymorphisms (SNPs) previously identified as gout risk loci or associated with serum urate (SU) concentration in the East Asian population were genotyped. Weighted polygenic risk scores were calculated to assess the cumulative effect of genetic risks on the subtypes. RESULTS:Of the 4,873 participants, 8.8% had an ROL subtype, 60.9% RUE subtype, 23.1% combined subtype, and 7.2% normal subtype. The ROL subtype was independently associated with older age at onset, lower SU, tophi, and diabetes mellitus; RUE was associated with lower body mass index (BMI) and non-diabetes mellitus; the combined subtype was associated with younger age at onset, higher BMI, SU, estimated glomerular filtration rate (eGFR), and smoking; and the normal subtype was independently associated with older age at onset, lower SU, and eGFR. Thirteen SNPs were associated with gout with 6 shared loci and subtype-dependent risk loci patterns. High polygenic risk scores were associated with ROL subtype (odds ratio [OR] = 9.63, 95% confidence interval [95% CI] 4.53-15.12), RUE subtype (OR = 2.18, 95% CI 1.57-3.03), and combined subtype (OR = 6.32, 95% CI 4.22-9.48) compared with low polygenic risk scores. CONCLUSION:Hyperuricemia subtypes classified according to renal uric acid handling have subtype-specific clinical and genetic features, suggesting subtype-unique pathophysiologic mechanisms.

Objectives: To evaluate whether ultrasound findings of monosodium urate (MSU) crystal deposition predict frequent gout flares in index joints over 12 months. Methods: This single-center study enrolled people with at least one gout flare involving the MTP1, ankle or knee joint. The most painful or most frequently joint was identified as index joint for analysis. All participants were started on urate-lowering therapy and had an ultrasound scan of the index joints at the baseline visit. OMERACT scores (for tophus, double contour sign and aggregates) were used to analyze whether ultrasound scores predicted frequent (>= 2) gout flares in the index joint over 12 months. Results: Frequent flares were significantly higher in those with ultrasound findings in all index joints (MTP1: tophus: 85.0% vs 46.0%, P < 0.001, aggregates: 78.8% vs 59.0%, P < 0.01; ankle: tophus: 54.6% vs 20.8%, P < 0.001; aggregates: 60.0% vs 35.9%, P < 0.05; knee: tophus: 68.4% vs 28.6%, P < 0.05). For the MTP1, for each 1-point increase in tophus score, the odds of frequent gout flares increased by 5.19 [(95%CI: 1.26-21.41), 7.91 [(95%CI: 2.23-28.14), and 13.79 [(95%CI: 3.79-50.20)] fold respectively. For the ankle, a tophus score of 3 markedly improved the prediction of the frequent flares [OR= 9.24 (95%CI=2.85-29.91)]. Semi-quantitative sum scores were associated with frequent flares with an OR (95%CI) of 13.66 (3.44-54.18), P < 0.001 at the MTP1, 7.05 (1.98-25.12), P < 0.001 at the ankle. Conclusion: Ultrasound features of MSU crystal deposition at the MTP1 and knee predict subsequent risk of frequent gout flares in the same joints following initiation of urate-lowering therapy, with the highest risk in those with high tophus scores.

Objective:This study aimed to understand predictors of inadequate response (IR) to low-dose febuxostat treatment based on clinical variables.Methods:We pooled data from 340 patients of an observational cohort and two clinical trials who received febuxostat 20 mg/day for at least 3 months. IR was defined as failure to reach the target serum urate level (sUA<6 mg/dL) at any time point during 3 months treatment. The potential predictors associated with short- or mid-term febuxostat IR after pooling the three cohorts were explored using mixed-effect logistic analysis. Machine learning models were performed to evaluate the predictors for IR using the pooled data as the discovery set and validated in an external test set.Results:Of the 340 patients, 68.9% and 51.8% were non-responders to low-dose febuxostat during short- and mid-term follow-up, respectively. Serum urate and triglyceride (TG) levels were significantly associated with febuxostat IR, but were also selected as significant features by LASSO analysis combined with age, BMI, and C-reactive protein (CRP). These five features in combination, using the best-performing stochastic gradient descent classifier, achieved an area under the receiver operating characteristic curve of 0.873 (95% CI [0.763, 0.942]) and 0.706 (95% CI [0.636, 0.727]) in the internal and external test sets, respectively, to predict febuxostat IR.Conclusion:Response to low-dose febuxostat is associated with early sUA improvement in individual patients, as well as patient age, BMI, and levels of TG and CRP.

The pathogenic causes of primary gout include urate overproduction and/or renal or extra-renal urate underexcretion. The aim of this study was to evaluate the association of gout subtypes with the response to low-purine diet (LPD). This is a single-center prospective clinical study. Gout patients visiting from 2019 to 2022, from Shandong Gout Clinic Center at the Affiliated Hospital of Qingdao University, China, assigned to three groups according to clinical subtypes, were enrolled and all treated with 2-week low-purine diet. General characteristics, serum uric acid (sUA) and other clinical biochemical variables before and after the diet were evaluated. A total of 626 gout patients (age 41.20 ± 13.41 years, male 98.0

INTRODUCTION:The aim of the study was to explore the causes and clinical significance of hyperechoic renal medulla observed by ultrasonography in patients with primary gout. METHODS:This study included 2,107 patients with primary gout treated in the Gout Clinic of our hospital from 2016 to 2022. The clinical data and biochemical data of these patients were collected and analyzed. According to the presence or absence of punctate hyperechogenicity in the renal medulla on ultrasound examination, the patients were divided into the hyperechoic medulla (HM) and the normal hypoechoic medulla (NM) groups, and the HM group was further divided into the partial HM (P-HM) and fulfilled HM (F-HM) subgroups according to the distribution range of hyperechogenicity. RESULTS:Among the 2,107 patients with primary gout, 380 had hyperechoic renal medulla on renal ultrasound, including 106 patients with F-HM and 274 with P-HM. There were significant differences in the gout duration, urate arthropathy number, serum urate (SU) level, clinical tophi number, blood urea nitrogen, serum creatinine (sCr), and estimated glomerular filtration rate between the HM and NM groups or between the F-HM and P-HM subgroups (p < 0.05). Multivariate regression analysis showed that the presence of HM was positively correlated with gout duration, urate arthropathy number, gout attack frequency, SU, and sCr. The number of clinical tophi and sCr were closely related to F-HM. CONCLUSION:Ultrasound examination showed that a high medulla echo in patients with gout was often related to renal function damage. P-HM may be a transitory condition between NM and F-HM in patients with gout.

Objective: Adolescent-onset gout has a greater impact on the lives and health of patients than adult-onset gout. However, there is a relative lack of clinical information on adolescent-onset gout. Hence, we analyzed a Chinese cohort. Methods: We studied clinical features of 9,003 Chinese patients. Gout onset age of 12 - 19 years is defined as adolescent-onset group (AG), 20 - 40 years as early-onset group (EG), and 41 - 64 years as late-onset group (LG). Multivariable regression analysis evaluated factors associated with recurrent flares, serum urate (SU) levels, and underexcretion type in AG. Results: Compared with EG and LG, the AG had higher SU levels [AG: 9.5 (2.2) mg/dL, EG: 8.6 (2.1) mg/dL, LG: 7.73 (2.0) mg/dL, P < 0.001], higher percentage of positive family history of gout (AG: 41.8 %, EG: 29.6 %, LG: 24.6 %, P < 0.001), underexcretion type (AG: 62.4 %, EG: 62.5 %, LG: 58.8 %, P = 0.04), recurrent flares (AG: 78.1 %, EG: 70.3 %, LG: 68.9 %, P = 0.01). Urate-lowering therapy (ULT) initiated [OR 6.58 (95 % CI 1.35 - 32.00)] and hypercholesterolemia [OR 4.16 (95 % CI 1.28 - 13.53)] were associated with recurrent flares. eGFR was identified to be a significant variable of increasing SU levels [beta -0.24 (95 % CI -0.04 to -0.01)]. Hypertriglyceridemia [OR 0.35 (95 % CI 0.17 - 0.71)] was related to underexcretion type. Conclusion: Adolescent-onset gout patients had clinically distinctive features with higher SU levels, BMI, positive gout family history, underexcretion type and recurrent flares. These specific populations were less likely to achieve ULT target, requiring more clinical attention.