What it measures.
Uric acid is the end product of purine metabolism. When serum urate exceeds its solubility threshold (~6.8 mg/dL), monosodium urate crystals can deposit in joints (causing gout), kidneys (causing stones), and blood vessels. Beyond gout, elevated uric acid is independently associated with hypertension, cardiovascular disease, chronic kidney disease, and metabolic syndrome — making it a broader metabolic risk marker than commonly appreciated.
The concentration of uric acid (urate) in serum. Uric acid is produced from the breakdown of purines (from dietary intake and endogenous cell turnover) by the enzyme xanthine oxidase. Approximately two-thirds is excreted by the kidneys and one-third by the gut. Impaired excretion (kidney disease, medications, genetics) is the primary cause of hyperuricaemia in most cases.
Why it matters.
Uric acid above 6.8 mg/dL represents supersaturation — crystals can form at any time. Gout affects ~4% of adults and is the most common inflammatory arthritis. But uric acid also correlates with cardiovascular events, CKD progression, and metabolic syndrome independent of traditional risk factors. Treating hyperuricaemia with urate-lowering therapy prevents gout flares and may reduce kidney disease progression.
Physiology.
Purines from diet (red meat, organ meats, shellfish, beer) and endogenous cell turnover are metabolised to hypoxanthine → xanthine → uric acid by xanthine oxidase. Unlike most mammals, humans lack uricase (the enzyme that breaks down uric acid), so we rely entirely on renal and intestinal excretion. This evolutionary quirk means humans are uniquely susceptible to hyperuricaemia.
Testing & preparation.
How to prepare
- Fasting preferred (high-purine meals transiently elevate uric acid)
- Avoid alcohol for 24 hours (especially beer — high in purines)
- Note all medications — diuretics (thiazides, furosemide) and low-dose aspirin raise uric acid
- Dehydration can elevate uric acid — stay normally hydrated
When to test
Acute joint swelling (gout suspected). Recurrent kidney stones. Metabolic syndrome assessment. CKD monitoring. Cardiovascular risk assessment. Before and during diuretic therapy.
How often
During gout management: every 3-6 months until target reached, then annually. Otherwise as part of metabolic assessment.
Interpretation.
High uric acid
Common causes:
- Decreased renal excretion (most common): CKD, dehydration, medications (diuretics, cyclosporine)
- Increased production: high-purine diet, alcohol (especially beer), fructose, cell turnover (psoriasis, haemolysis, tumour lysis)
- Genetic predisposition (URAT1 transporter variants)
- Metabolic syndrome / insulin resistance (insulin reduces renal urate excretion)
- Lead nephropathy (saturnine gout)
Implications:
- >6.8 mg/dL: supersaturation — crystal formation possible; gout risk increases
- >9.0 mg/dL: high risk of gout flare and urate nephropathy
- Paradox: uric acid may be NORMAL during acute gout attack (inflammation drives excretion)
- Chronic hyperuricaemia: independent risk factor for hypertension, CKD progression, and cardiovascular events
- Associated with insulin resistance regardless of BMI
Low uric acid
Common causes:
- Severe liver disease (reduced purine metabolism)
- Fanconi syndrome (renal tubular wasting)
- SIADH (dilutional)
- Xanthine oxidase inhibitor therapy (allopurinol, febuxostat) — therapeutic goal
- Wilson's disease
- Very low purine diet (rare)
Implications:
- Low uric acid is uncommon and usually clinically insignificant
- Very low (<2.0 mg/dL) may warrant investigation for renal tubular disorders
Optimization.
Diet
- Limit high-purine foods: organ meats, red meat, shellfish, sardines, anchovies
- Limit alcohol, especially beer (high in purines) and spirits
- Limit fructose and sugar-sweetened beverages (fructose metabolism generates uric acid)
- Cherries and cherry juice: modest urate-lowering effect (some evidence)
- Coffee consumption associated with lower uric acid (observational)
- Dairy products (low-fat) associated with lower gout risk
Lifestyle
- Weight loss reduces uric acid (insulin resistance is a major driver)
- Stay well hydrated (2-3L/day) — dilutes urine and promotes urate excretion
- Regular exercise (but avoid dehydration during intense exercise)
- Review medications: switch thiazide diuretics if possible; losartan has uricosuric properties
Supplements
- Vitamin C (500-1000mg/day): modest uricosuric effect
- No supplement replaces urate-lowering therapy when indicated
FAQs.
My uric acid is high but I've never had gout — should I worry?
Asymptomatic hyperuricaemia doesn't routinely require medication, but it increases future gout risk and is associated with cardiovascular disease, CKD, and metabolic syndrome. Lifestyle modification (diet, weight loss, hydration) is reasonable. Medication is typically started after a second gout attack or if complications exist.
Why was my uric acid normal during my gout attack?
This is a well-known paradox. During acute inflammation, the kidneys temporarily increase urate excretion, dropping serum levels. Up to 40% of acute gout attacks have 'normal' uric acid. Recheck 2-4 weeks after the flare resolves for an accurate baseline.
Does diet really make a difference?
Diet alone typically lowers uric acid by 1-2 mg/dL — meaningful but often insufficient if levels are significantly elevated. The biggest dietary contributors are alcohol (especially beer), fructose, and organ meats. Weight loss has a larger effect than specific food avoidance. Most patients with recurrent gout ultimately need medication.