Uric acid and cardiovascular diseases: a reappraisal

ABSTRACT

Serum uric acid (SUA) has garnered an increased interest in recent years as an important determinant of cardiovascular disease. Uric acid, a degradation product of purine metabolism, is affected by several inheritable and acquired factors, such as genetic mutation, metabolic syndrome, chronic kidney disease, and medication interactions. Even though elevated SUA have been commonly associated with the development of gout, it has significant impact in the development of hypertension, metabolic syndrome, and cardiovascular disease. Uric acid, in both crystalline and soluble forms, plays a key role in the induction of inflammatory cascade and development of atherosclerotic diseases. This concise reappraisal emphasizes key features about the complex and challenging role of uric acid in the development and progression of atherosclerosis and cardiovascular disease. It explores the pathogenesis and historical significance of uric acid, highlights the complex interplay between uric acid and components of metabolic syndrome, focuses on the pro-inflammatory and pro-atherogenic effects of uric acid, as well as discusses the role of urate lowering therapies in mitigating the risk of cardiovascular disease while providing the latest evidence to the healthcare professionals focusing on the clinical importance of SUA levels with regards to cardiovascular disease.

KEYWORDS:

• Serum uric acid
• hyperuricemia
• cardiovascular disease
• metabolic syndrome
• urate lowering therapies
• hypertension

Declaration of financial/other relationships

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties. Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.