Serum urate as a predictor of cardiovascular risk in coronary artery disease

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Created On: 12/05/2025

Elevated serum urate (SU) levels are linked to a heightened risk of cardiovascular (CV) events, mortality, and the development of gout.

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Key take away

Serum urate strongly forecasts MACE, overall mortality, and cardiovascular-related death in coronary artery disease. These associations persist despite IL-1β blockade and vary based on kidney function and gout.

Background

Elevated serum urate (SU) levels are linked to a heightened risk of cardiovascular (CV) events, mortality, and the development of gout. This study sought to explore whether SU serves as a predictor for CV risk in patients undergoing interleukin (IL)-1β inhibition with canakinumab and to check whether IL-1β blockade, kidney function, or the presence of gout modify these relationships.

Method

This analysis was a subset of the Canakinumab Antiinflammatory Thrombosis Outcome Study (CANTOS). It involved 10,061 individuals with a history of myocardial infarction and raised levels of high-sensitivity C-reactive protein. Volunteers were randomly segregated to get one of three doses of canakinumab or a placebo. SU levels were monitored at baseline.

For evaluating the impact of SU on outcomes, Cox proportional hazards models were employed to compare major adverse cardiovascular events (MACE), CV death, and all-cause mortality among participants with SU levels categorized as normal (≤6.8 mg/dL), elevated (6.8 to 9.0 mg/dL), or markedly elevated (≥9.0 mg/dL). Subgroup analyses were executed based on treatment group (canakinumab vs. placebo), kidney function (estimated glomerular filtration rate [eGFR] ≥60 vs. <60 mL/min), and gout status (yes vs. no).

Result

Those with elevated SU levels faced a noticeably higher risk of MACE (hazard ratio [HR]: 1.66), CV death (HR: 2.52), and all-cause mortality (HR: 2.43) when compared to those with normal SU levels. Even after adjusting for key confounders, SU was an independent determinant of all three outcomes. These findings remained consistent regardless of IL-1β blockade with canakinumab. For those with normal kidney function (eGFR ≥60), SU was linked with increased CV and all-cause mortality, but not with MACE. Those with gout experienced higher rates of adverse events, regardless of their SU levels.

Conclusion

In the cohort of over 10,000 patients with coronary artery disease, markedly elevated SU levels were a strong indicator of increased CV risk, even when treated aggressively. IL-1β blockade did not markedly alter these links. Kidney function and the presence of gout appeared to influence the impact of SU on CV outcomes.