Prevalence and metabolic risk factors of chronic kidney disease among a Mexican adult population: a cross-sectional study in primary healthcare medical units.

Introduction: The intricate relationship between obesity and chronic kidney disease (CKD) progression underscores a significant public health challenge. Obesity is strongly linked to the onset of several health conditions, including arterial hypertension (AHTN), metabolic syndrome, diabetes, dyslipidemia, and hyperuricemia. Understanding the connection between CKD and obesity is crucial for addressing their complex interplay in public health strategies. Objective: This research aimed to determine the prevalence of CKD in a population with high obesity rates and evaluate the associated metabolic risk factors. Material and Methods: In this cross-sectional study conducted from January 2017 to December 2019 we included 3,901 participants of both sexes aged ≥20 years who were selected from primary healthcare medical units of the Mexican Social Security Institute (IMSS) in Michoacan, Mexico. We measured the participants' weight, height, systolic and diastolic blood pressure, glucose, creatinine, total cholesterol, triglycerides, HDL-c, LDL-c, and uric acid. We estimated the glomerular filtration rate using the Collaborative Chronic Kidney Disease Epidemiology (CKD-EPI) equation. Results: Among the population studied, 50.6% were women and 49.4% were men, with a mean age of 49 years (range: 23-90). The prevalence of CKD was 21.9%. Factors significantly associated with an increased risk of CKD included age ≥60 years (OR = 11.70, 95% CI [9.83-15.93]), overweight (OR = 4.19, 95% CI [2.88-6.11]), obesity (OR = 13.31, 95% CI [11.12-15.93]), abdominal obesity (OR = 9.25, 95% CI [7.13-11.99]), AHTN (OR = 20.63, 95% CI [17.02-25.02]), impaired fasting glucose (IFG) (OR = 2.73, 95% CI [2.31-3.23]), type 2 diabetes (T2D) (OR = 14.30, 95% CI [11.14-18.37]), total cholesterol (TC) ≥200 mg/dL (OR = 6.04, 95% CI [5.11-7.14]), triglycerides (TG) ≥150 mg/dL (OR = 5.63, 95% CI 4.76-6.66), HDL-c <40 mg/dL (OR = 4.458, 95% CI [3.74-5.31]), LDL-c ≥130 mg/dL (OR = 6.06, 95% CI [5.12-7.18]), and serum uric acid levels ≥6 mg/dL in women and ≥7 mg/dL in men (OR = 8.18, 95% CI [6.92-9.68]), (p < 0.0001). These factors independently contribute to the development of CKD. Conclusions: This study underscores the intricate relationship between obesity and CKD, revealing a high prevalence of CKD. Obesity, including overweight, abdominal obesity, AHTN, IFG, T2D, dyslipidemia, and hyperuricemia emerged as significant metabolic risk factors for CKD. Early identification of these risk factors is crucial for effective intervention strategies. Public health policies should integrate both pharmacological and non-pharmacological approaches to address obesity-related conditions and prevent kidney damage directly.

Effects of the concentration of seeds, finite time-dependent supersaturations, and viscosity on the crystallization kinetics of monosodium urate monohydrate.

CONTEXT: Although the crystallization of monosodium urate monohydrate (MSUM) has a crucial role in the occurrence of gout, which is an inflammatory arthritis disease, theoretical models have not been able to describe all features observed in its seeded growth kinetics. In contrast to previous modeling approaches, we show that our model can reproduce qualitative features typically observed in experiments. In particular, our results show that the higher the initial supersaturation and the lower the viscosity, the faster the crystallization kinetics, and they also indicate that there are distinct growth regimes for low and high concentrations of seeds. METHODS: In this work, we introduce an alternative approach based on a master equation that allows us to incorporate hypotheses for the seeded growth crystallization of MSUM in a more transparent way. Such an approach includes not only effects that are related to the finite time-dependent supersaturation and concentration of seeds, but it can also be used to determine how the viscosity of the solution can affect the crystallization kinetics of MSUM molecules.

Unveiling overlooked pathways: The uric acid catabolism genes in the human genome.

In hominids, including Homo sapiens, uric acid is the end product of purine catabolism. In contrast, other placental mammals further degrade uric acid to (S)-allantoin by enzymes such as urate oxidase (uricase), HIU hydrolase (HIUase), and OHCU decarboxylase. Some organisms, such as frogs and fish, hydrolyze (S)-allantoin to allantoate and eventually to (S)-ureidoglycolate and urea, while marine invertebrates convert urea to ammonium. In H. sapiens, mutations in the uricase gene led to a reduction in the selective pressure for maintaining the integrity of the genes encoding the other enzymes of the purine catabolism pathway, resulting in an accumulation of uric acid. The hyperuricemia resulting from this accumulation is associated with gout, cardiovascular disease, diabetes, and preeclampsia. Many commonly used drugs, such as aspirin, can also increase uric acid levels. Despite the apparent absence of these enzymes in H. sapiens, there appears to be production of transcripts for uricase (UOX), HIUase (URAHP), OHCU decarboxylase (URAD), and allantoicase (ALLC). While some URAHP transcripts are classified as long non-coding RNAs (lncRNAs), URAD and ALLC produce protein-coding transcripts. Given the presence of these transcripts in various tissues, we hypothesized that they may play a role in the regulation of purine catabolism and the pathogenesis of diseases associated with hyperuricemia. Here, we specifically investigate the unique aspects of purine catabolism in H. sapiens, the effects mutations of the uricase gene, and the potential regulatory role of the corresponding transcripts. These findings open new avenues for research and therapeutic approaches for the treatment of hyperuricemia and related diseases.

The potential relationship between uric acid and the recovery in sudden sensorineural hearing loss.

OBJECTIVE: Serum uric acid is proven to be associated with chronic hearing loss, but its effect on Sudden Sensorineural Hearing Loss (SSNHL) is unclear. This study aims to evaluate the prognostic values of serum uric acid levels in SSNHL patients. METHODS: The clinical records of SSNHL patients were retrospectively reviewed. Patients were divided into different groups based on hearing recovery and audiogram type, and uric acid levels were compared. Based on uric acid levels, patients were categorized into normouricemia and hyperuricemia groups, and clinical features and hearing recovery were evaluated. Univariate and multivariate analyses were performed to identify prognostic factors. RESULTS: In total, 520 SSNHL patients were included in this study, including 226 females and 294 males. In female patients, 186 patients were included in the normouricemia group, and 40 patients were enrolled in the hyperuricemia group. Significant differences were observed in uric acid levels, Total Cholesterol (TC), rate of complete recovery, and slight recovery between the two groups. In male patients, 237 subjects were categorized into the normouricemia group, and 57 patients were included in the hyperuricemia group. The rate of complete recovery and slight recovery was lower in the hyperuricemia group compared to the normouricemia group. All patients were further divided into good recovery and poor recovery groups based on hearing outcomes. The uric acid levels, initial hearing threshold, rate of hyperuricemia, and TC were lower in the good recovery group than the poor recovery group both in female and male patients. Binary logistic regression results showed that uric acid levels, initial hearing threshold, and hyperuricemia were associated with hearing recovery. CONCLUSION: Hyperuricemia might be an independent risk factor for hearing recovery in SSNHL patients. Serum uric acid and initial hearing threshold possibly affected the hearing outcome in males and females with SSNHL. LEVEL OF EVIDENCE: Level 4.

The potential relationship between uric acid and the recovery in sudden sensorineural hearing loss

Abstract Objective Serum uric acid is proven to be associated with chronic hearing loss, but its effect on Sudden Sensorineural Hearing Loss (SSNHL) is unclear. This study aims to evaluate the prognostic values of serum uric acid levels in SSNHL patients. Methods The clinical records of SSNHL patients were retrospectively reviewed. Patients were divided into different groups based on hearing recovery and audiogram type, and uric acid levels were compared. Based on uric acid levels, patients were categorized into normouricemia and hyperuricemia groups, and clinical features and hearing recovery were evaluated. Univariate and multivariate analyses were performed to identify prognostic factors. Results In total, 520 SSNHL patients were included in this study, including 226 females and 294 males. In female patients, 186 patients were included in the normouricemia group, and 40 patients were enrolled in the hyperuricemia group. Significant differences were observed in uric acid levels, Total Cholesterol (TC), rate of complete recovery, and slight recovery between the two groups. In male patients, 237 subjects were categorized into the normouricemia group, and 57 patients were included in the hyperuricemia group. The rate of complete recovery and slight recovery was lower in the hyperuricemia group compared to the normouricemia group. All patients were further divided into good recovery and poor recovery groups based on hearing outcomes. The uric acid levels, initial hearing threshold, rate of hyperuricemia, and TC were lower in the good recovery group than the poor recovery group both in female and male patients. Binary logistic regression results showed that uric acid levels, initial hearing threshold, and hyperuricemia were associated with hearing recovery. Conclusion Hyperuricemia might be an independent risk factor for hearing recovery in SSNHL patients. Serum uric acid and initial hearing threshold possibly affected the hearing outcome in males and females with SSNHL. Level of evidence Level 4.

Relationship between hyperuricemia, HSP70 and NLRP3 inflammasome in arterial hypertension / La relación hiperuricemia-HSP70-NLRP3 inflamosoma en la hipertensión arterial

Abstract Arterial hypertension is the most important cardiovascular risk factor in chronic non-communicable diseases and is estimated to be responsible for 10.4 million deaths annually. The global prevalence of hypertension is 30% and the majority of people with hypertension do not have a clear identifiable cause and are considered to have primary hypertension. Experimental and clinical investigations from several research groups, including ours, have established that inflammation and autoimmune reactivity play a role in the sodium retention and hemodynamic responses that drive primary hypertension. Hyperuricemia and heat stress proteins (HSP), particularly HSP70, are both associated with the activation of innate immunity that plays a role in the development of inflammatory reactivity in the hypertensive patient. Clinical studies have shown an association between the expression of HSP70 and anti-HSP70 antibodies and primary hypertension. This brief review aims to examine the interrelation between hyperuricemia and extracellular overexpression of HSP70 in the activation of the inflammasome that may have a central role in the pathophysiology of primary hypertension.

Resumen La hipertensión arterial es el factor de riesgo cardiovascular más importante de las enfermedades crónicas no transmisibles y se estima que es responsable de 10.4 millones de muertes al año. La prevalencia mundial de la hipertensión es del 30%; la mayoría de las personas con hipertensión no tienen una causa claramente identificable y se considera que tienen hipertensión primaria. Las investigaciones experimentales y clínicas de varios grupos de investigación, incluido el nuestro, han establecido que la inflamación y la reactividad autoinmune desempeñan un papel en la retención de sodio y las respuestas hemodinámicas que provocan la hipertensión primaria. La hiperuricemia y las proteínas del estrés por calor (HSP), particularmente HSP70, están asociadas con la activación de la inmunidad innata que juega un papel en el desarrollo de la reactividad inflamatoria en pacientes hipertensos. Estudios clínicos han demostrado asociación entre la expresión de HSP70 y anticuerpos anti-HSP70 y la hipertensión arterial primaria Esta breve revisión tiene como objetivo examinar la interrelación entre la hiperuricemia y la sobreexpresión extracelular de HSP70 en la activación del inflamasoma, así como su probable papel central en la fisiopatología de la hipertensión primaria.

Relationship between hyperuricemia, HSP70 and NLRP3 inflammasome in arterial hypertension.

Arterial hypertension is the most important cardiovascular risk factor in chronic non-communicable diseases and is estimated to be responsible for 10.4 million deaths annually. The global prevalence of hypertension is 30% and the majority of people with hypertension do not have a clear identifiable cause and are considered to have primary hypertension. Experimental and clinical investigations from several research groups, including ours, have established that inflammation and autoimmune reactivity play a role in the sodium retention and hemodynamic responses that drive primary hypertension. Hyperuricemia and heat stress proteins (HSP), particularly HSP70, are both associated with the activation of innate immunity that plays a role in the development of inflammatory reactivity in the hypertensive patient. Clinical studies have shown an association between the expression of HSP70 and anti-HSP70 antibodies and primary hypertension. This brief review aims to examine the interrelation between hyperuricemia and extracellular overexpression of HSP70 in the activation of the inflammasome that may have a central role in the pathophysiology of primary hypertension.

La hipertensión arterial es el factor de riesgo cardiovascular más importante de las enfermedades crónicas no transmisibles y se estima que es responsable de 10.4 millones de muertes al año. La prevalencia mundial de la hipertensión es del 30%; la mayoría de las personas con hipertensión no tienen una causa claramente identificable y se considera que tienen hipertensión primaria. Las investigaciones experimentales y clínicas de varios grupos de investigación, incluido el nuestro, han establecido que la inflamación y la reactividad autoinmune desempeñan un papel en la retención de sodio y las respuestas hemodinámicas que provocan la hipertensión primaria. La hiperuricemia y las proteínas del estrés por calor (HSP), particularmente HSP70, están asociadas con la activación de la inmunidad innata que juega un papel en el desarrollo de la reactividad inflamatoria en pacientes hipertensos. Estudios clínicos han demostrado asociación entre la expresión de HSP70 y anticuerpos anti-HSP70 y la hipertensión arterial primaria Esta breve revisión tiene como objetivo examinar la interrelación entre la hiperuricemia y la sobreexpresión extracelular de HSP70 en la activación del inflamasoma, así como su probable papel central en la fisiopatología de la hipertensión primaria.

Autosomic Dominant Tubulo Interstitial Kidney Disease: Case Report of a New Variant of the UMOD Gene.

Autosomal dominant tubulointerstitial kidney disease (ADTKD) is a low-prevalence pathology mainly associated with pathogenic variants of the UMOD gene. It is characterized by the progressive deterioration of renal function, associated with hyperuricemia and accompanied by a family history of gout or hyperuricemia. Often, clinical variability and a lack of molecular testing results in diagnostic failure to determine the ADTKD-UMOD association. Case presentation: We describe the case of a 14-year-old male who presented to the nephrology service with hyperuricemia, renal ultrasonographic changes, and progression to chronic kidney disease in 4 years. He had a family history of hyperuricemia. A probable genetic disease with an autosomal dominant inheritance pattern was considered, confirmed by the presence of a probably pathogenic variant of the UMOD gene, not previously reported in the literature. Conclusion: The investigation of this case led to the identification of a new variant in the UMOD gene, broadening the spectrum of known variants for ADTKD-UMOD. In addition, in this case, a comprehensive anamnesis, that takes into account family history, was the key point to carry out genetic tests that confirmed the diagnosis suspicion. Directed Genetic tests are currently an essential diagnostic tool and should be performed as long as they are available and there is an indication to perform them.

Anti-Hyperuricemic, Anti-Arthritic, Hemolytic Activity and Therapeutic Safety of Glycoconjugated Triazole-Phthalimides.

Hyperuricemia, the metabolic alteration that leads to gout or gouty arthritis, is increasing worldwide. Glycoconjugated triazole-phthalimides show potent anti-inflammatory activity. The aim of this study was to evaluate the anti-hyperuricemia effect of glycoconjugated triazole-phthalimides. To develop hyperuricemia, groups of mice received orally potassium oxonate (250 mg/kg) for 7 days, and F2, F3 and F4 glycoconjugated triazole-phthalimides (20 mg/kg), allopurinol (300 mg/kg), and 1% carboxymethylcellulose; indomethacin (2 and 4 mg/kg) was the positive control for anti-arthritic effect. Genotoxic and mutagenic effects were evaluated by the comet and micronucleus assays, respectively. The hemolytic action of the compounds was evaluated. Phthalimides F2, F3 and F4 significantly reduced the levels of serum uric acid, creatinine and urea in hyperuricemic animals. In addition, the compounds were efficient in reducing protein denaturation in a dose-dependent manner. In an interesting way, the histopathological analysis of kidneys from groups treated with F2, F3 and F4 showed a glomerular architecture, with the Bowman's capsule and renal tubules having a normal appearance and without inflammatory changes. Also, F2 and F4 showed a small increase in micronuclei, indicating a low mutagenic effect, whilst by comet assay only, we could infer that F4 affected the frequency and damage index, thus indicating a very small genotoxic action. Similarly, the phthalimides showed a low degree of erythrocyte hemolysis (<3%). Our data demonstrate that the new glycoconjugate triazole-phthalimides have potential to treat hyperuricemia and its secondary complications, such as gouty arthritis, with a low to non-significant rate of erythrocytes hemolysis, genotoxicity and mutagenicity making these molecules strong candidates as pharmaceutical agents for treatment requiring uric-acid-lowering therapy.

Osthole Prevents Heart Damage Induced by Diet-Induced Metabolic Syndrome: Role of Fructokinase (KHK).

There is increasing evidence that either ingested or produced fructose may have a role in metabolic syndrome. While not commonly considered a criterion for metabolic syndrome, cardiac hypertrophy is often associated with metabolic syndrome, and its presence carries increased cardiovascular risk. Recently it has been shown that fructose and fructokinase C (KHK) can be induced in cardiac tissue. Here we tested whether diet-induced metabolic syndrome causes heart disease associated with increased fructose content and metabolism and whether it can be prevented with a fructokinase inhibitor (osthole). Male Wistar rats were provided a control diet (C) or high fat/sugar diet for 30 days (MS), with half of the latter group receiving osthol (MS+OT, 40 mg/kg/d). The Western diet increased fructose, uric acid, and triglyceride concentrations in cardiac tissue associated with cardiac hypertrophy, local hypoxia, oxidative stress, and increased activity and expression of KHK in cardiac tissue. Osthole reversed these effects. We conclude that the cardiac changes in metabolic syndrome involve increased fructose content and its metabolism and that blocking fructokinase can provide cardiac benefit through the inhibition of KHK with modulation of hypoxia, oxidative stress, hypertrophy, and fibrosis.

Analysis of the prevalence and influencing factors of hyperuricemia in children and adolescents aged 6-17 years in northeastern Sichuan Province.

OBJECTIVE: To investigate the factors influencing hyperuricemia in children and adolescents and to provide a scientific basis for early prevention and treatment. METHODS: A retrospective study (2017-2021) of the prevalence of hyperuricemia in children and adolescents was conducted, and the factors influencing hyperuricemia were analyzed by multi-factor logistic regression. RESULTS: The overall prevalence of hyperuricemia in children and adolescents aged 6-17 years in northeast Sichuan Province was 55.12% (8676/15,739), of which 60.68% (5699/9392) in boys and 46.90% (2977/6347) in girls; the prevalence of hyperuricemia from 2017 to 2021 was 52.40% ( 1540/2939), 52.56% (1642/3124), 52.11% (1825/3502), 58.33% (1691/2899), and 60.40% (1978/3275), respectively; the prevalence rates of 6-12 years old were 48.92% (864/1766), 50.46% (769/1524), and 52.73% (685/1299), 56.99% (693/1216), 35.46% (444/1252), 46.33% (524/1131), 60.50% (720/1190), and 66.82% (739/1106), 58.95% (652/1106), and 62.17% (761/1106) for 13-17 years old, respectively, 62.17% (761/1224), 63.19% (855/1353), and 61.70% (970/1572), respectively. Logistic regression showed that the prevalence of male (OR = 1.451, 95% CI 1.034 to 2.035, p = 0.031), age (OR = 1.074, 95% CI 1.024 to 1.126, p = 0.003), overweight/obesity (OR = 1.733, 95% CI 1.204∼2.494, p = 0.003), blood creatinine (OR = 1.018, 95% CI 1.005∼1.031, p = 0.007), triglycerides (OR = 1.450, 95% CI 1.065∼1.972, p = 0.018), blood calcium (OR = 6.792, 95% CI 1.373∼33.594, p = 0.019), and systolic blood pressure (OR = 1.037, 95% CI 1.018∼1.057, p < 0.001) were influential factors for the development of hyperuricemia. CONCLUSION: The prevalence of hyperuricemia was higher in children and adolescents aged 6-17 years in northeastern Sichuan Province, with a higher prevalence in boys than in girls, and the prevalence increased with age.

Senescent CD4+CD28null cells are increased in chronic hyperuricemia, show aberrant effector phenotypes, and are reversed after allopurinol therapy: a proof-of-concept pilot study.

To characterize CD4+CD28null cells in chronic hyperuricemia and investigate whether allopurinol could restore CD28 expression and the balance of T helper phenotypes. Asymptomatic individuals with chronic hyperuricemia and ultrasonographic findings evocative of urate deposition in the joints. Age- and gender-matched normouricemic individuals were also studied. Oral allopurinol at 150 mg/day for 4 weeks, followed by 300 mg/day through week 12. Color-flow cytometry on peripheral blood mononuclear cells (PBMC) with antibodies against CD4, CD28, T-bet (Th1), GATA-3 (Th2), and RORγt (Th17). Six patients (five men, median age of 53 years) and seven controls were studied. At baseline, hyperuricemic patients had more CD4+CD28null/CD4+ cells than normouricemic subjects (36.8% vs. 6.1%; p = 0.001), with a predominance of T-bet+ cells (98.5% vs. 6.6%; p = 0.001) and few RORγt+ cells (0.7% vs. 89.4%; p = 0.014). In hyperuricemic patients, the number of CD4+ cells/10,000 PBMC was similar before and after allopurinol (3378 vs. 3954; p = 0.843). Conversely, CD4+CD28null cells decreased from 36.8% (23.0-43.7) to 15.8% (4.7-28.1; p = 0.031). CD4+CD28nullT-bet+ cells decreased from 98.5% (95.0-99.4) to 88.3% (75.2-98.9; p = 0.062), CD4+CD28nullGATA-3+ cells increased from 0% (0-4.0) to 2.8% (0.1-15.6; p = 0.156), and CD4+CD28nullRORγt+ cells increased from 0.7% (0.4-7.0) to 4.5% (1.3-28.1; p = 0.031). The CD4+CD28null cell subset is abnormally expanded in chronic hyperuricemia, despite the absence of overt urate-related disease. Allopurinol may partially restore CD28 expression on CD4+ cells while enhancing the homeostatic balance of T helper phenotypes. ClinicalTrials.gov, number NCT04012294.

Nutritional, biochemical, and clinical determinants of hyperuricemia in systemic lupus erythematosus patients: Relationship with clinical and renal disease activity.

Systemic lupus erythematosus (SLE) is the prototypical autoimmune disease considered as an independent risk factor for mortality by cardiovascular disease. Currently, uric acid is described as a novel biomarker associated with cardiometabolic risk. However, nutritional and serum determinants that influence hyperuricemia development in autoimmune diseases have not been fully elucidated. This study aimed to assess the nutritional, biochemical, and cardiometabolic determinants of hyperuricemia and its relationship with clinical variables in SLE patients. A cross-sectional study was conducted in 167 SLE patients and 195 control subjects (CS). Nutrient intake, anthropometry, biochemical, and cardiometabolic indexes were evaluated. In SLE patients, adequate protein (OR = 0.4; p = 0.04) and carbohydrate (OR = 0.2; p = 0.01) intakes were associated with a lower risk of hyperuricemia. SLE patients with hyperuricemia presented a higher risk of clinical (OR = 2.2; p = 0.03) and renal activity (OR = 3.4; p < 0.01), as well as triglycerides ≥150 mg/dL (OR = 3.6; p < 0.01), hs-CRP ≥1 mg/L (OR = 3.1; p < 0.01), Kannel score ≥3 (OR = 2.5; p = 0.02), and BMI ≥25 kg/m2 (OR = 2.2; p = 0.02). Oppositely, serum levels of HDL-C ≥40 mg/dL (OR = 0.2; p < 0.01) were associated with a lower risk of hyperuricemia. According to the pharmacotherapy administered, prednisone treatment was associated with a high risk of hyperuricemia (OR = 4.7; p < 0.001). In contrast, the hydroxychloroquine treatment was associated with a lower risk of hyperuricemia (OR = 0.4; p = 0.02). In conclusion, SLE patients with hyperuricemia presented a high risk of clinical and renal activity as well as worse cardiometabolic status. Notably, an adequate intake of protein, carbohydrates, healthy HDL-C serum levels, and hydroxychloroquine treatment could be determinants of lower risk of hyperuricemia.

Ultra-processed foods: Cross-sectional and longitudinal association with uric acid and hyperuricemia in ELSA-Brasil.

BACKGROUND AND AIMS: Food intake influences uric acid (UA) levels and hyperuricemia (HU), but evidence on the role of ultra-processed foods (UPFs) are scarce. The association between UPFs consumption and (1) HU prevalence and UA levels; (2) HU cumulative incidence; and (3) UA level change over a 4-year period was investigated. METHODS AND RESULTS: Cross-sectional and longitudinal analyses were performed using baseline (2008-2010, aged 35-74 years) and second visit (2012-2014) data from the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil). Participants with glomerular filtration rate <60 mL/min/1.73 m2, bariatric surgery, implausible caloric intake, and using urate-lowering therapy (ULT) at baseline were excluded (all analyses). Participants with HU at baseline were excluded from longitudinal analyses. UPFs consumption was assessed using a food frequency questionnaire (FFQ) and categorized by the NOVA classification system (100 g/day). HU was defined as UA≥6.8 mg/dL. Linear, logistic, and mixed-effect linear regressions investigated the associations between UPFs consumption and UA/HU, adjusted for covariates. The final samples included 13,923 (cross-sectional) and 10,517 (longitudinal) individuals. The prevalence of HU was 18.7%, and the cumulative incidence was 4.9%. Greater UPFs consumption was associated with a greater prevalence of HU (OR:1.025 95%CI: 1.006; 1.044) and higher UA levels (ß:0.024 95%CI: 0.016; 0.032). Every additional consumption of 100 g/day of UPFs raised the 4-year cumulative incidence of HU by 5.6% (95%CI: 1.021; 1.092). However, UPFs were not associated with the pace of UA level changes during the study period. CONCLUSION: The present study shows that greater UPFs consumption is associated with another deleterious health consequence: higher UA levels and the risk of having HU.

Hyperuricemia: an unrecognized risk factor for kidney-related sequelae in children with hemolytic uremic syndrome.

BACKGROUND: Chronic kidney-related sequelae after STEC-HUS occur in 20-40% of patients. Hyperuricemia (HU) may cause acute and chronic toxicity involving the kidneys. We retrospectively assessed if there was an association between the presence of HU during the acute illness and that of kidney-related sequelae in children with STEC-HUS. METHODS: Children with STEC-HUS who had clinical and laboratory data at 2 years of follow-up were included in this case-control study. Univariate and multivariate analyses were performed between patients with (cases) or without (controls) kidney-related sequelae to identify factors associated with outcomes, including different measures of serum uric acid (sUA) (baseline level, peak, and duration of HU). HU was defined as sUA > 8 mg/dL. RESULTS: Of 86 patients included, 77.9% had HU. Patients with sequelae (n = 41) had a higher prevalence of HU (41/41 vs. 26/45, p < 0.01), higher baseline leukocyte count, serum creatinine (sCr), and sUA levels as well as lower sodium than controls. During hospitalization, cases also had higher sCr peak, sUA peak and duration of HU, requirement and duration of dialysis, extrarenal complications, and hypertension. By multivariate analysis, after adjusting for length of dialysis, only duration of HU (p = 0.0005; OR 1.7, 95% CI 1.27-2.36) remained as an independent predictor of sequelae, with a best cutoff of 5.5 days (AUC 0.95, specificity 80%, sensitivity 100%). CONCLUSIONS: The presence of HU is a common finding in children with STEC-HUS and its duration during the acute stage was associated with kidney-related sequelae, regardless of the duration of dialysis. A higher resolution version of the Graphical abstract is available as Supplementary Information.

Analysis of the prevalence and influencing factors of hyperuricemia in children and adolescents aged 6-17 years in northeastern Sichuan Province

Abstract Objective: To investigate the factors influencing hyperuricemia in children and adolescents and to provide a scientific basis for early prevention and treatment. Methods: A retrospective study (2017-2021) of the prevalence of hyperuricemia in children and adolescents was conducted, and the factors influencing hyperuricemia were analyzed by multifactor logistic regression. Results: The overall prevalence of hyperuricemia in children and adolescents aged 6-17 years in northeast Sichuan Province was 55.12% (8676/15,739), of which 60.68% (5699/9392) in boys and 46.90% (2977/6347) in girls; the prevalence of hyperuricemia from 2017 to 2021 was 52.40% ( 1540/2939), 52.56% (1642/3124), 52.11% (1825/3502), 58.33% (1691/2899), and 60.40% (1978/ 3275), respectively; the prevalence rates of 6-12 years old were 48.92% (864/1766), 50.46% (769/1524), and 52.73% (685/1299), 56.99% (693/1216), 35.46% (444/1252), 46.33% (524/1131), 60.50% (720/1190), and 66.82% (739/1106), 58.95% (652/1106), and 62.17% (761/1106) for 13-17 years old, respectively, 62.17% (761/1224), 63.19% (855/1353), and 61.70% (970/1572), respectively. Logistic regression showed that the prevalence of male (OR = 1.451, 95% CI 1.034 to 2.035, p = 0.031), age (OR = 1.074, 95% CI 1.024 to 1.126, p = 0.003), overweight/obesity (OR = 1.733, 95% CI 1.204~2.494, p = 0.003), blood creatinine (OR = 1.018, 95% CI 1.005~1.031, p = 0.007), triglycerides (OR = 1.450, 95% CI1.065~1.972, p = 0.018), blood calcium (OR = 6.792, 95% CI 1.373~33.594, p = 0.019), and systolic blood pressure (OR = 1.037, 95% CI 1.018~1.057, p < 0.001) were influential factors for the development of hyperuricemia. Conclusion: The prevalence of hyperuricemia was higher in children and adolescents aged 6-17 years in northeastern Sichuan Province, with a higher prevalence in boys than in girls, and the prevalence increased with age.

Cardiometabolic Risk Factors in Mexican Adults With Congenital Heart Disease.

Background: In recent decades, adults living with congenital heart disease (ACHD) have improved their survival, thus increasing their predisposition to the onset of cardiometabolic risk factors and chronic health conditions. Objectives: The purpose of this study was to describe cardiometabolic risk profiles in the ACHD population and their relationship to congenital heart disease (CHD) lesion complexity. Methods: We performed a cross-sectional study from ACHD in a third-tier referral center in Mexico City. The association between cardiometabolic risk factors and CHD complexity was estimated using logistic regression models. Results: Our study cohort included 1,171 ACHD patients (median age: 31 [IQR: 23.2-42.7] years, male 63.6%). Cardiac diagnosis was classified as mild (44.9%), moderate (37.8%), and severe (17.2%) CHD complexity. Low high-density lipoprotein cholesterol (55%) was the most common cardiometabolic risk factor; followed by insulin resistance (54.5%) and prediabetes (52.4%). Patients with mild and moderate CHD had a higher prevalence of obesity and metabolic syndrome, while patients with severe CHD had a higher prevalence of hyperuricemia and subclinical hypothyroidism. In the logistic regression analysis, the severity of CHD was associated with higher odds of hyperuricemia (moderate CHD, OR: 1.87; 95% CI: 1.20-2.93; P = 0.010; severe CHD, OR: 2.75; 95% CI: 1.64-4.62; P < 0.001) and lower risks of metabolic syndrome (OR: 0.61; 95% CI: 0.41-0.91; P = 0.010), prediabetes (OR: 0.58; 95% CI: 0.42-0.81; P < 0.001), and arterial hypertension (OR: 0.49; 95% CI: 0.33-0.74; P < 0.001) compared with mild CHD complexity. Conclusions: We observed high rates of cardiometabolic risk factors in Mexican ACHD patients and these risk profiles varied by CHD lesion complexity. These results highlight the need for ongoing metabolic health surveillance in the ACHD population.

Tofo gotoso gigante en presentación inusual / Giant gouty tophi in unusual presentation

La gota es una enfermedad reumática inflamatoria que se debe al depósito de cristales de urato monosódico en las articulaciones. En su evolución clínica se distingues dos formas: la fase aguda caracterizada por un proceso inflamatorio monoarticular agudo de gran sensibilidad, y la fase crónica o de mantenimiento, cuyo elemento fundamental es la acumulación de cristales de urato monosódico llamados tofos gotosos. Estos se presentan con mayor frecuencia en el dorso de los dedos, a nivel articular y en el pabellón auricular. Se presenta el caso de un paciente masculino, de 47 años, con diagnóstico de gota de 5 años de evolución y con tratamiento irregular. Este paciente presentó tofos gotosos en localizaciones infrecuentes que limitaron su capacidad funcional. Este caso demuestra la necesidad de un diagnóstico oportuno y una adecuada adherencia al tratamiento, por lo que se considera importante para la comunidad médica, especialmente los profesionales de la salud que atienden a pacientes con artropatía gotosa(AU)´

Gout is a rheumatic, inflammatory disease that is generated by the deposition of monosodium urate crystals at the joint level. Two forms can be distinguished in its clinical evolution: the acute phase characterized by an acute monoarticular inflammatory process of great sensitivity, and the chronic or maintenance phase where the fundamental element is the presence of accumulations of monosodium urate crystals called gouty tophi. These occur more frequently on the back of the fingers, at the joint level and in the auricle. This paper presents the case of a 47-year-old male patient, diagnosed with gout for 5 years and with irregular treatment, who presented gouty tophi in infrequent locations that limit the patient's functional capacity. The case is presented considering it important for the medical community; especially health professionals caring for patients with gouty arthropathy(AU)´

Asociación entre uricemia y síndrome metabólico en un centro hospitalario de Corrientes / Association between uricemia and metabolic syndrome in a hospital center in Corrientes

Resumen Introducción: en los últimos años numerosa evidencia científica sugiere que la hiperuricemia puede jugar un papel en el desarrollo del síndrome metabólico (SM). En algunos estudios se ha explorado la asociación entre la uricemia y la presencia de SM. Sin embargo, aún no está del todo esclarecido si altos niveles del ácido úrico se relacionan de una manera causal con el desarrollo del SM. Más aún, existen pocos estudios acerca de la presencia del SM y su relación con los niveles de AU en la ciudad de Corrientes. Objetivos: determinar la relación de los niveles séricos de AU y los parámetros que definen el SM en pacientes que concurren al consultorio externo de Clínica Médica y Medicina General del Hospital Ángela I. de Llano, Corrientes, Argentina. Resultados: se incluyó un total de 435 pacientes mayores de 18 años: 312 mujeres (72%) y 123 hombres (28%). El 58% de la población cumplía con el criterio de SM del NCEP-ATP III (60% mujeres y 52% hombres). El 75% presentó hiperuricemia y SM. En este estudio la presencia de SM se asoció significativamente con los valores de uricemia OR: 1.5 (IC 95%: 1,3-1,8). La asociación fue estadísticamente significativa. Conclusiones: los resultados demostraron que el aumento de la frecuencia de los componentes del SM está en relación directa con el incremento de los niveles séricos de AU, y que el valor de corte para esta asociación fue de 4 mg/dl; de ahí la importancia de considerar la determinación de los niveles séricos de AU como posible predictor de SM.

Abstract Introduction: in recent years, numerous scientific evidence suggest that hyperuricemia may play a role in the development of metabolic syndrome (MS). Some studies have explored the association between uricemia and the presence of MS. However, it remains unclear whether high uric acid levels are causally related to the development of MS. Moreover, there are few studies on the presence of metabolic syndrome and its relationship with uric acid (UA) levels in the city of Corrientes, Argentina. Objectives: to determine the relationship between serum UA levels and the parameters that define MS in patients attending the outpatient clinic of Medical Clinic and General Medicine of the Ángela I. de Llano Hospital, Corrientes. Results: a total of 435 patients over 18 years of age were included: 312 (72%) women and 123 (28) men. Fifty-eight percent of the population met the NCEP-ATP III criteria for MS (60% females and 52% males). Seventy-five percent of the population had hyperuricemia and MS. In this study the presence of MS was significantly associated with uricemia values OR:1.5 (95%CI:1.3-1.8). The association is statistically significant. Conclusions: the results show that the increase in the frequency of the components of MS, goes in direct relation with the increase in serum UA levels and that the cut-off value for this association is 4 mg/dl. Hence the importance of considering the determination of serum UA levels as a possible predictor of MS.

Serum uric acid is a predictive biomarker of incident metabolic syndrome at the Brazilian longitudinal study of adult Health (ELSA - Brasil).

AIM: To investigate whether serum uric acid (SUA) levels and hyperuricemia can be predictive biomarkers of incident metabolic syndrome(MS) among different body mass index(BMI) categories, and to investigate SUA cutoffs that best discriminate individuals with incident MS. METHODS: We analyzed 7,789 participants without MS at baseline of ELSA-Brasil study. Logistic regression models were performed to evaluate associations between incident MS and SUA levels/hyperuricemia, expressed by odds ratios(ORs) and confidence intervals(95 % CI). RESULTS: We found 1,646 incident MS cases after a median follow-up of 3.8[3.5-4.1] years. Incident MS was present among 8.3 % (n = 290) of participants with normal weight, 28.3 % (n = 850) with overweight, 39.8 % (n = 506) with obesity. Among incident MS participants of total sample, 33.0 % had hyperuricemia [SUA > 6.0 mg/dL (356.9 µmol/L)]. After all adjustments, SUA was independently prognostic of incident MS: for each 1 mg/dL increase in SUA the odds of incident MS were 45 % higher (OR1.45[CI95 %1.34-1.55 p <.01]). Associations were found for those presenting normal weight, overweight and obesity (OR1.43[CI95 %1.31-1.57 p <.01; OR1.22[CI95 %1.13-1.32 p <.01]; and OR1.16[CI95 %1.04-1.29 p <.05]) respectively. Hyperuricemia was independently associated with incident MS (OR1.88[CI95 %1.49-0.2.36 p <.01]). The SUA cut point level maximizing sensitivity and specificity in the discrimination of incident MS was 5.0 mg/dL. CONCLUSIONS: SUA level is an independent predictive biomarker of incident MS at all BMI categories.