Uric acid as a cardiorenal mediator: pathogenesis and mechanistic insights

Introduction: The role of serum uric acid as a connector in cardiorenal interactions has been long debated and studied extensively in the past decade. Epidemiological, and clinical data suggest that hyperuricemia may be an independent risk factor as well as a strong predictor of morbidity and mortality in cardiovascular diseases (CVD) and renal diseases. New data suggesting that urate lowering therapies may improve outcomes in cardiovascular diseases have generated interest. Areas Covered: This review attempts to summarize the pathophysiological mechanisms by which hyperuricemia causes cardiorenal dysfunction. It also provides a summary of the recent evidence for urate lowering therapies and the possible underlying mechanisms which lead to cardiovascular benefits. This was a narrative review with essential references or cross references obtained via expert opinion. Expert Opinion: Emphasis on newer drugs that address the cardio-renal metabolic axis and the relation to their effects on uric acid may help further elucidate underlying mechanisms responsible for their cardiovascular and renal benefits. Once these benefits are well established, we will be able to come up with guidelines for targeting hyperuricemia. This can potentially lead to a change in clinical practice and can possibly lead to improved cardiovascular and renal outcomes.

Automated summary

This review summarizes the pathophysiological mechanisms of how hyperuricemia causes cardiorenal dysfunction and provides a summary of recent evidence for urate lowering therapies. Emphasis on newer drugs that address the cardio-renal metabolic axis and their effects on uric acid may help elucidate underlying mechanisms responsible for cardiovascular and renal benefits.