Objective: To examine the relationships of serum uric acid concentration with several risk factors of cardiovascular diseases (CVD).
Subjects: 957 men 18 y old participating in the Verona Young Men Atherosclerosis Risk Factors Study, a cross-sectional population-based study.
Measurements: Body mass index (BMI), waist/hip ratio (WHR), serum uric acid, serum lipids, blood pressure, fasting insulin and behavioural variables.
Results: Serum uric acid concentration showed positive associations with BMI (r = 0.24; P < 0.0001), WHR (r = 0.19; P < 0.0001) and serum triglyceride levels (r = 0.19; P < 0.0001); it was also significantly correlated to systolic (r = 0.08; P < 0.01) and diastolic (r = 0.11; P < 0.001) blood pressure, fasting insulin (r = 0.11; P < 0.001), total (r = 0.12; P < 0.001) and LDL cholesterol (r = 0.10; P < 0.01) plasma concentrations. Life-style characteristics, such as smoking and physical activity did not show any significant association, while daily alcohol intake was positively associated with uric acid concentration (r = 0.09; P < 0.01). While the adjustment for fasting insulin did not substantially change these results, the magnitude of the correlations between uric acid and CVD risk factors markedly decreased when allowance was made for BMI and WHR. Only triglycerides maintained an independent correlation with uric acid levels (r = 0.17; P < 0.0001). In multivariate regression analysis, serum triglycerides, BMI and WHR (at borderline significance) were independent positive predictors of uric acid (R2 of the model 0.122, P < 0.001), while fasting insulin concentration did not give any independent contribution to explain the variability uric acid levels.
Conclusions: These data indicate that, already in young, essentially health subjects, hyperuricaemia associates with several components of the so-called insulin resistance syndrome, thus suggesting that increased levels of uric acid might be another member of this syndrome. In addition, these data suggest that obesity and central body fat distribution, rather than hyperinsulinaemia/insulin resistance, play a major role in linking hyperuricaemia with CVD risk factors clustering in the insulin resistance syndrome. Nevertheless, hypertrigliceridemia is related to hyperuricemia independently of obesity and central body fat distribution.
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Scientifica (Cairo)
January 2025
Department of Pharmaceutical Sciences, North South University, Dhaka, Bangladesh.
In chronic kidney disease (CKD), hyperuricemia is a common phenomenon, presumably due to reduced renal clearance of uric acid. This study investigated the effect of xanthine oxidase (XO) inhibitors allopurinol and febuxostat to prevent oxidative stress in the kidney of two-kidney, one-clip (2K1C) rats. In this investigation, 2K1C rats were used as an experimental animal model for kidney dysfunction.
View Article and Find Full Text PDFBMC Nephrol
January 2025
Department of Nephrology, Jinshan Hospital Affiliated to Fudan University, Shanghai, China.
Background: To explore the prevalence of hyperuricemia and its associated factors in uremic patients undergoing maintenance hemodialysis (MHD).
Methods: Two hundred two uremic patients undergoing MHD for ≥ 3 months, in Jinshan Hospital, Fudan University, were enrolled. Pre-dialysis blood samples were tested during March 1st, 2023 to April 30th, 2023.
Hipertens Riesgo Vasc
January 2025
EAP Gòtic, Barcelona, Spain. Electronic address:
Curr Opin Nephrol Hypertens
January 2025
Department of Urology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Purpose Of Review: Metabolic dysfunction associated steatotic liver disease (MASLD) is increasing throughout the world, affecting nearly one in three individuals. Kidney stone disease, which is also increasing, is associated with MASLD. Common risk factors for both, including obesity, diabetes, dyslipidemia, hypertension, and metabolic syndrome, are likely drivers of this association.
View Article and Find Full Text PDFArterioscler Thromb Vasc Biol
January 2025
Department of Cardiovascular Medicine, The University of Tokyo, Bunkyo-ku, Japan. (H. Yagi, H.A., Q.L., A.S.-K., M.U., H.K., R.M., A.S., S.O., H.T., Norifumi Takeda, I.K.).
Background: Marfan syndrome (MFS) is an inherited disorder caused by mutations in the gene encoding fibrillin-1, a matrix component of extracellular microfibrils. The main cause of morbidity and mortality in MFS is thoracic aortic aneurysm and dissection, but the underlying mechanisms remain undetermined.
Methods: To elucidate the role of endothelial XOR (xanthine oxidoreductase)-derived reactive oxygen species in aortic aneurysm progression, we inhibited in vivo function of XOR either by endothelial cell (EC)-specific disruption of the gene or by systemic administration of an XOR inhibitor febuxostat in MFS mice harboring the missense mutation p.
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