Uric acid in heart failure: a biomarker or therapeutic target?

There is a need for a cost-effective prognostic biomarker in heart failure (HF). Substantial evidence suggests that uric acid (UA) is an independent marker for adverse prognosis in acute and chronic HF of varying severity. Whether UA is a merely a marker of poor prognosis or is an active participant in disease pathogenesis is currently unknown. In the setting of HF, at least two different processes can be responsible for increased UA: increased production, which may result from oxidative stress, and decreased excretion due to renal insufficiency, which can be a consequence of cardio-renal syndrome, renal congestion, or comorbidities. While pioneer studies have raised the possibility of preventing HF through the use of UA lowering agents, namely xanthine oxidase inhibitors and uricosurics, the literature is still conflicting on whether the reduction in UA will result in a measurable clinical benefit. In this review, we examine the evidence relating UA to HF prognosis, the mechanisms that contribute to increased UA levels in HF, and future novel treatments aimed at reducing UA levels.