For clinicians
Uric acid
- Unit
- mg/dL
What is Uric acid?
Uric acid arises from the breakdown of substances called 'purines', from food and your own cells. Your kidneys normally clear it away neatly. Staying neatly within range prevents crystals from building up in joints. It's also linked to your metabolism and blood pressure.
Clinical frame
Uric acid is the end product of purine metabolism and has a dual profile: an important antioxidant in plasma, but pro-oxidant inside the cell and in an atherosclerotic plaque. Soluble uric acid activates the innate immune system through the NLRP3 inflammasome and NF-κB, raising IL-1β, IL-6 and TNF-α, even without crystal formation [1].
In a dose-response meta-analysis of 39 studies with over a million participants, hyperuricaemia was associated with about 20% more coronary heart disease and 75% more cardiovascular mortality, with 16% extra risk per unit increase [2].
Causality is not proven: genetically elevated uric acid does cause gout, but not diabetes, coronary heart disease, stroke or heart failure [3]. Uric acid is therefore mainly a risk marker that refines the cardiometabolic and inflammatory profile, alongside the other metabolic parameters [3].
What moves this value?
Lots of red meat, organ meat, alcohol (especially beer) and sugary drinks can raise it. Heredity plays a part.
Less alcohol and sugary drinks, more water and a varied diet help lower it over the weeks.
Developed and reviewed with the Synapse medical advisory board.
References
- Joosten, L. A. B., Crişan, T. O., Bjornstad, P. & Johnson, R. J. Asymptomatic hyperuricaemia: a silent activator of the innate immune system. Nat Rev Rheumatol 16, 75–86 (2020). doi.org/10.1038/s41584-019-0334-3
- Lyu, D. et al. Association of hyperuricemia with coronary heart disease and other cardiovascular outcomes: a systematic review and dose-response meta-analysis. PLoS One 20, e0337091 (2025). doi.org/10.1371/journal.pone.0337091
- Keenan, T. et al. Causal assessment of serum urate levels in cardiometabolic diseases through a Mendelian randomization study. J Am Coll Cardiol 67, 407–416 (2016). doi.org/10.1016/j.jacc.2015.10.086
The colour zones are personal: they depend on age, sex, risk and history, and appear in the patient's own report.
Insights to discuss with the patient, not a diagnostic instrument.