During the last century, there has been an increasing prevalence of hyperuricaemia noted in many populations. While uric acid is usually discussed in the context of gout, hyperuricaemia is also associated with hypertension, chronic kidney disease, hypertriglyceridaemia, obesity, atherosclerotic heart disease, metabolic syndrome, and type 2 diabetes. Here we review the connection between hyperuricaemia and cardiovascular, kidney and metabolic diseases. Contrary to the popular view that uric acid is an inert metabolite of purine metabolism, recent studies suggest serum uric acid may have a variety of pro-inflammatory, pro-oxidative and vasoconstrictive actions that may contribute to cardiometabolic diseases. Hyperuricaemia is a predictive factor for the development of hypertension, metabolic syndrome, type 2 diabetes, coronary artery disease, left ventricular hypertrophy, atrial fibrillation, myocardial infarction, stroke, heart failure and chronic kidney disease. Treatment with uric acid-lowering therapies has also been found to improve outcomes in patients with hypertension and kidney disease, in some but not all studies. In conclusion, uric acid is emerging as a potentially treatable risk factor for cardiometabolic diseases, and more clinical trials investigating the potential benefit of lowering serum uric acid are recommended in individuals with hyperuricaemia with and without deposition and concomitant hypertension, metabolic syndrome or chronic kidney disease.
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http://dx.doi.org/10.1016/j.ejim.2020.07.006 | DOI Listing |
Am J Cardiovasc Drugs
January 2025
Division of Cardiology, Department of Internal Medicine, Ilsan Paik Hospital, Inje University College of Medicine, Goyang, Republic of Korea.
Background: Amiodarone is an effective anti-arrhythmic drug; however, it is frequently associated with thyroid dysfunction. The aim of this study was to investigate the incidence and risk factor of amiodarone-induced dysfunction in an iodine-sufficient area.
Methods: This retrospective cohort study included 27,023 consecutive patients treated with amiodarone for arrhythmia, using the Korean National Health Insurance database.
Clin Pharmacokinet
January 2025
Clinical Pharmacology and Toxicology Service, Anesthesiology, Pharmacology and Intensive Care Department, Geneva University Hospitals, 4 Rue Gabrielle Perret-Gentil, 1205, Geneva, Switzerland.
Background And Objective: Fexofenadine is commonly used as a probe substrate to assess P-glycoprotein (Pgp) activity. While its use in healthy volunteers is well documented, data in older adult and polymorbid patients are lacking. Age- and disease-related physiological changes are expected to affect the pharmacokinetics of fexofenadine.
View Article and Find Full Text PDFPediatr Nephrol
January 2025
Department of Paediatrics, University Medical Centre Maribor, Ljubljanska ulica 5, 2000, Maribor, Slovenia.
Background: Serum and urinary uromodulin are emerging as potential cardiovascular risk factors. The aim of our study was to determine uromodulin in both serum and urine to evaluate their potential as early cardiovascular risk markers and markers of kidney function in children and young adults.
Methods: This case-control study included 72 participants - 42 children and young adults with chronic kidney disease stages 1-2 and 30 healthy controls.
Funct Integr Genomics
January 2025
School of Medical Technology, Tianjin Medical University, Tianjin, 300203, China.
Clear cell renal cell carcinoma (ccRCC) is a highly malignant tumor characterized by a significant propensity for recurrence and metastasis. DNA methylation has emerged as a critical epigenetic mechanism with substantial utility in cancer diagnosis. In this study, multi-omics data were utilized to investigate the target genes regulated by the transcription factor MYC-associated zinc finger protein (MAZ) in ccRCC, leading to the identification of thymidine phosphorylase (TYMP) as a gene with notably elevated expression in ccRCC.
View Article and Find Full Text PDFInflamm Res
January 2025
Department of Nephrology, First Affiliated Hospital of Naval Medical University, Shanghai Changhai Hospital, Shanghai, China.
Background: Chronic inflammation is well recognized as a key factor related to renal function deterioration in patients with diabetic kidney disease (DKD). Neutrophil extracellular traps (NETs) play an important role in amplifying inflammation. With respect to NET-related genes, the aim of this study was to explore the mechanism of DKD progression and therefore identify potential intervention targets.
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