Biomarker µmol/l (mg/dl)

Uric Acid

End product of purine metabolism – marker for gout risk and metabolic syndrome

Also known as

serum uric acid urate hyperuricemia marker

Definition

Uric acid is the end product of purine breakdown in humans (lacking the uricase enzyme found in other mammals). It is produced mainly from endogenous purine metabolism (cell nucleus breakdown) and from dietary purines (red meat, organ meats, beer, fructose). Elevated uric acid (hyperuricemia) is the primary risk factor for gout and is associated with metabolic syndrome, cardiovascular disease, and kidney stones.

Parameter Value
Unit µmol/l (mg/dl)
Reference Range Women: 150–350 µmol/l (2.5–5.9 mg/dl) | Men: 200–420 µmol/l (3.4–7.0 mg/dl)
Optimal Range (lab2go) Women: < 300 µmol/l (< 5 mg/dl) | Men: < 360 µmol/l (< 6 mg/dl) (lab2go Optimum Zone — well below crystallization threshold; < 360 µmol/l is the EULAR gout treatment target)

Conversion: 1 mg/dl = 59.5 µmol/l. US labs report in mg/dl (Women 2.0–7.0, Men 3.4–7.2 mg/dl).

What a low value means

Very low uric acid (< 120 µmol/l / < 2 mg/dl) can occur with molybdenum cofactor deficiency (very rare), Fanconi syndrome (renal tubular defect), SIADH, or xanthinuria. Uric acid also has antioxidant properties extracellularly — very low levels are controversially associated with increased Parkinson's risk.

What a high value means

Hyperuricemia (> 420 µmol/l / > 7 mg/dl) increases risk of gout attacks (urate crystal arthritis), urolithiasis (uric acid stones), chronic nephropathy, and cardiovascular disease. Associated with metabolic syndrome, insulin resistance, and fructose-rich diet.

How to optimize this marker

Diet: reduce purine-rich foods (organ meats, red meat, shellfish, beer). Strongly limit fructose (HFCS, sodas) — fructose-induced uric acid production. Drink plenty of water (2–3 l/day promotes renal uric acid excretion). Coffee (uricosuric effect). Vitamin C (500–1,000 mg/day) increases renal excretion.

When to test

For gout history, joint pain, kidney stones, metabolic syndrome, kidney insufficiency, or medication review (diuretics, low-dose aspirin, cyclosporine raise uric acid). Fasting measurement recommended.

Frequently asked questions

Does a ketogenic diet worsen uric acid? +

Short-term, a ketogenic diet can raise uric acid because ketone bodies compete with uric acid for renal excretion. Longer term (> 6 months), uric acid often normalizes through weight loss and fructose reduction. Individual monitoring is recommended with a history of hyperuricemia.

What is the difference between asymptomatic hyperuricemia and gout? +

Asymptomatic hyperuricemia: elevated uric acid (> 420 µmol/l) without symptoms. Treatment is debated; in high-risk patients (> 540 µmol/l, kidney insufficiency), allopurinol may be considered. Gout: episodic, acutely inflammatory arthritis from urate crystal deposits in joints — medication indicated (colchicine, allopurinol/febuxostat).

Is fruit juice really worse than beer for uric acid? +

Beer contains purines (yeast) and raises uric acid through two mechanisms. Fruit juices (apple, orange, grape) with high fructose content raise uric acid through fructose-dependent ATP degradation. Alcohol also reduces renal uric acid excretion. Both are problematic; sugar-sweetened beverages (HFCS) carry the strongest dietary risk for hyperuricemia.

Does uric acid have any beneficial properties? +

Yes. Uric acid is a potent antioxidant extracellularly and contributes approximately 50% of plasma antioxidant capacity. Epidemiological studies associate low uric acid with increased Parkinson's and MS risk. This explains the paradox: uric acid is pathogenic (gout) yet low levels show potentially increased neurodegenerative risk.

Last Reviewed: May 28, 2026 · sina

This information is for orientation only and does not replace medical advice. Reference ranges can vary by laboratory, method and country.