Uric Acid Test

What is a Uric Acid test?

Uric acid is a waste product formed when your body breaks down purines: substances found in red meat, organ meats, shellfish, alcohol (especially beer) and some vegetables. Normally the kidneys filter uric acid out in urine. When production is too high or kidneys are underperforming, uric acid builds up (hyperuricaemia), forming crystals that deposit in joints and cause gout, or in the kidneys, causing kidney stones.

Uric Acid Normal Range

What does HIGH uric acid mean?

What is Gout?

What does LOW uric acid mean?

Questions to ask your doctor

• Do I need medication or just dietary changes?
• Which foods should I specifically avoid?
• Should I check my kidney function too?
• How much water should I drink daily?

Frequently asked questions

References

The clinical information on this page is drawn from peer-reviewed sources indexed by the US National Library of Medicine. Links go to the source so you can read it yourself.

1. Hyperuricemia. In: StatPearls. Treasure Island (FL): StatPearls Publishing. NCBI Bookshelf NBK459218

References

Sources cited on this page. PubMed links open the original abstract.

1. Choi HK, Atkinson K, Karlson EW, Curhan G. Obesity, weight change, hypertension, diuretic use, and risk of gout in men. Arch Intern Med. 2005;165(7):742–748. PMID 15596918 · doi:10.1001/archinte.165.7.742

Uric acid and cardiovascular risk – the emerging picture

For most of the 20th century, uric acid was thought of purely as a marker of gout and kidney stones. Over the past two decades, a large body of epidemiological evidence has linked hyperuricaemia with hypertension, metabolic syndrome, chronic kidney disease, and cardiovascular events – even in individuals who never develop gout. Serum uric acid above 6 mg/dL (357 µmol/L) is associated with a 26% increased risk of incident hypertension and up to 65% higher risk of cardiovascular mortality in some meta-analyses.

Whether this represents a causal relationship or pure association (because uric acid travels with insulin resistance and renal dysfunction) remains debated. Current evidence does not support urate-lowering therapy purely for cardiovascular protection, but it reinforces that elevated uric acid should prompt a cardiovascular risk assessment rather than be dismissed as irrelevant until gout develops.

The treat-to-target approach for gout

Modern gout management is built around a serum urate target. Current NICE (NG219) and British Society for Rheumatology guidelines recommend a target serum urate below 360 µmol/L (6 mg/dL) for most patients – and below 300 µmol/L (5 mg/dL) in those with tophi, frequent flares, or chronic gouty arthropathy. This level is below the saturation point of monosodium urate crystals, promoting dissolution of existing deposits.

Allopurinol (a xanthine oxidase inhibitor) is the first-line urate-lowering drug. The dose is typically started at 100 mg daily and titrated upward every 4 weeks guided by serum urate testing, to a maximum of 900 mg/day. Febuxostat is an alternative for patients intolerant of allopurinol. A major pitfall is starting urate-lowering therapy during an acute attack – this can prolong or worsen the flare by mobilising urate crystals; treatment should generally start after the flare has settled, with prophylactic colchicine or low-dose NSAID cover for 3–6 months.

False results – what raises and lowers the result artifactually

High dietary purine intake (red meat, organ meats, shellfish, beer) raises uric acid acutely. Fasting for 24 hours before the test improves consistency. Aspirin at low doses (75–300 mg/day) paradoxically reduces uric acid excretion and raises serum levels; high-dose aspirin has the opposite uricosuric effect. Diuretics – particularly thiazides and loop diuretics – are a common and clinically important cause of hyperuricaemia and gout. Cyclosporin (used after organ transplants) causes gout in a large proportion of transplant recipients.