Uric acid mg/dL to µmol/L Converter

Uric acid in two units: the short answer

To convert uric acid from mg/dL to µmol/L, multiply by 59.48 (about 60). To convert µmol/L back to mg/dL, divide by 59.48. A uric acid of 6 mg/dL is therefore about 357 µmol/L, and 420 µmol/L is about 7.1 mg/dL. Some laboratories, particularly in the UK and Australia, report uric acid in mmol/L: 0.36 mmol/L is the same as 360 µmol/L. The converter above handles both directions and shows typical ranges and the gout treatment target.

Uric acid – also called urate or serum urate – is the key blood test for gout. The goals that guidelines set for people on urate-lowering treatment are expressed in both units, and because the two numbers look so different, mistakes are common when patients move between countries or read guidelines written for another system. This guide covers what uric acid is, how to convert it, normal ranges, the treatment target and the factors that change a result.

What uric acid is

Uric acid is the end product of the breakdown of purines – building blocks of DNA and RNA found in every cell and in many foods. Humans, unlike most mammals, lack the enzyme uricase that converts uric acid into a more soluble compound, so our levels are naturally higher. About two-thirds of uric acid is excreted by the kidneys and one-third through the gut.

At the pH of blood, uric acid exists mainly as its salt, monosodium urate. Above a concentration of about 6.8 mg/dL (405 µmol/L) at normal body temperature, urate exceeds its solubility limit and can form needle-shaped crystals. When crystals form in and around joints, they can trigger the intense inflammation of a gout attack. They can also form deposits called tophi under the skin and around joints, and contribute to kidney stones.

Having a raised uric acid level is called hyperuricemia. Most people with hyperuricemia never develop gout, but the higher and longer the level stays raised, the greater the risk.

mg/dL, µmol/L and mmol/L explained

• mg/dL is used in the United States and some other countries.
• µmol/L is the SI unit used in most of Europe, Canada and elsewhere.
• mmol/L is used by many laboratories in the UK, Australia and New Zealand. Move the decimal point three places: 0.42 mmol/L = 420 µmol/L.

Why the factor is 59.48

Uric acid's molar mass is 168.11 g/mol. A concentration of 1 mg/dL is 10 mg per liter, or 10,000 µg per liter, which is 10,000 ÷ 168.11 = 59.48 µmol/L. Many clinicians round to 60 for mental arithmetic, and some laboratories use 59.5.

How to convert uric acid step by step

1. Check whether the report uses mg/dL, µmol/L or mmol/L.
2. If it is mmol/L, multiply by 1,000 to get µmol/L.
3. From mg/dL, multiply by 59.48 to get µmol/L.
4. From µmol/L, divide by 59.48 to get mg/dL.
5. Round µmol/L to the nearest whole number and mg/dL to one decimal place.

Worked examples

• 5 mg/dL × 59.48 = 297 µmol/L (0.30 mmol/L) – the stricter target for severe gout.
• 6 mg/dL × 59.48 = 357 µmol/L (0.36 mmol/L) – the standard gout treatment target.
• 6.8 mg/dL × 59.48 = 404 µmol/L – the approximate saturation point of urate.
• 8 mg/dL × 59.48 = 476 µmol/L.
• 300 µmol/L ÷ 59.48 = 5.0 mg/dL.
• 0.45 mmol/L = 450 µmol/L ÷ 59.48 = 7.6 mg/dL.
• 540 µmol/L ÷ 59.48 = 9.1 mg/dL.

Mental shortcut

Multiply mg/dL by 60 (then subtract a little) or divide µmol/L by 60. For 7.5 mg/dL: 7.5 × 60 = 450; the exact value is 446 µmol/L.

Uric acid conversion chart

Normal uric acid ranges

Typical adult reference ranges are about 3.4–7.0 mg/dL (200–420 µmol/L) for men and 2.4–6.0 mg/dL (140–360 µmol/L) for women. Ranges vary by laboratory and population; some laboratories set the upper limit at 7.0 mg/dL for everyone.

Differences by sex and age

Before menopause, women have lower uric acid because oestrogen increases its excretion by the kidneys. After menopause, women's levels rise towards those of men, and gout becomes more common in older women. Children have lower levels than adults, with a rise at puberty, especially in boys. Uric acid tends to increase with age in both sexes, partly because of declining kidney function and medicines such as diuretics.

Why "normal" may not mean "healthy"

Reference ranges describe the levels seen in the general population, and because hyperuricemia is common, the upper limit of a population range can be higher than the solubility limit of urate. A man with a uric acid of 7.0 mg/dL (416 µmol/L) is within many laboratories' range but above the point where urate crystals can form. For people with gout, the treatment target is what matters, not the reference range.

The gout treatment target

Both the American College of Rheumatology (ACR, 2020) and the European Alliance of Associations for Rheumatology (EULAR, 2016 update) recommend a "treat-to-target" approach for people with gout who are on urate-lowering therapy such as allopurinol or febuxostat:

• Target below 6 mg/dL (360 µmol/L, 0.36 mmol/L) for everyone on urate-lowering treatment.
• Target below 5 mg/dL (300 µmol/L, 0.30 mmol/L) suggested by EULAR for people with severe gout – tophi, chronic arthritis or frequent attacks – until the crystals dissolve.
• EULAR also advises against keeping levels below 3 mg/dL (180 µmol/L) for the long term.

Keeping urate below the saturation point allows existing crystals to dissolve slowly, which over months to years reduces flares and shrinks tophi. Medicines are typically started at a low dose and increased step by step, with uric acid checked every few weeks until the target is reached. In the first months of treatment, flares can temporarily increase as crystals dissolve, so preventive anti-inflammatory treatment is usually given at the same time.

The UK's NICE guideline (2022) gives the same target of below 360 µmol/L, and below 300 µmol/L for people with tophi, chronic gouty arthritis or continued flares.

Uric acid during a gout attack

Uric acid levels can fall during an acute gout flare, sometimes into the normal range, because inflammation increases urate excretion. A normal level during an attack therefore does not rule out gout. If uric acid is used to support a diagnosis, it is best measured at least two weeks after the flare has settled. The gold standard for diagnosis is finding urate crystals in fluid taken from the joint.

Low uric acid

A uric acid below about 2 mg/dL (120 µmol/L) is uncommon. Causes include urate-lowering medicines, pregnancy, some kidney tubular disorders (such as Fanconi syndrome), syndrome of inappropriate antidiuretic hormone (SIADH), severe liver disease and rare inherited conditions. Low uric acid itself rarely causes symptoms.

What affects uric acid results

• Diet – foods rich in purines (organ meats, red meat, some seafood such as anchovies, sardines and shellfish), beer and spirits, and drinks sweetened with fructose or high-fructose corn syrup raise uric acid.
• Alcohol – especially beer, which contains purines and also reduces urate excretion.
• Body weight – obesity and insulin resistance raise uric acid; weight loss lowers it.
• Kidney function – reduced kidney function lowers excretion and raises uric acid.
• Medicines – thiazide and loop diuretics, low-dose aspirin, ciclosporin, tacrolimus, pyrazinamide and ethambutol raise uric acid. Losartan, fenofibrate and SGLT2 inhibitors modestly lower it, alongside allopurinol, febuxostat and probenecid.
• Rapid cell turnover – psoriasis, some blood cancers and chemotherapy (tumour lysis syndrome) increase uric acid production.
• Dehydration, fasting and intense exercise can raise levels temporarily.
• Genetics – variants in kidney urate transporters account for a large share of differences between people.

Diet and urate: how much difference does it make?

Dietary changes typically lower uric acid by around 1 mg/dL (60 µmol/L) or less – helpful, but rarely enough on its own to reach the treatment target in someone with established gout. Guidelines therefore recommend lifestyle measures alongside, not instead of, medication when medication is indicated. Cherries, coffee and low-fat dairy have been linked to lower urate or fewer flares in observational studies, but the effects are modest.

Monitoring uric acid on treatment

When urate-lowering treatment is started, uric acid is usually checked every two to five weeks while the dose is adjusted, then every six to twelve months once the target has been reached and maintained. A practical example shows why the units matter in this phase. Suppose a man starts allopurinol with a baseline level of 9.2 mg/dL. Four weeks later a laboratory in another country reports 0.41 mmol/L. Converted, that is 410 µmol/L or 6.9 mg/dL: a real improvement of about 25%, but still above the target of 6 mg/dL (360 µmol/L), so the dose would usually be increased further.

Allopurinol doses are often increased gradually from 100 mg a day, including in people with reduced kidney function, with careful monitoring. Febuxostat is an alternative when allopurinol is not tolerated or does not work. People of Han Chinese, Thai or Korean descent are often tested for the HLA-B*58:01 gene before starting allopurinol, because it is linked to a rare but severe skin reaction.

Uric acid and kidney stones

About 10% of kidney stones in many countries are made of uric acid, and the proportion is higher in people with gout, diabetes or obesity. Uric acid stones form mainly when urine is persistently acidic (pH below about 5.5), which reduces urate solubility; a high blood uric acid is not required. Treatment focuses on drinking enough fluid to produce at least 2–2.5 liters of urine a day and making the urine less acidic, often with potassium citrate. People with gout and kidney stones may need both their blood urate and their urine chemistry assessed.

Uric acid in pregnancy

Uric acid falls in early pregnancy as kidney filtration rises, then gradually climbs in the third trimester. A raised uric acid has long been associated with pre-eclampsia, but it is not a reliable test for diagnosing or predicting it, and current guidelines do not use it for that purpose. Pre-eclampsia is diagnosed from blood pressure and signs of organ involvement.

Uric acid beyond gout

Raised uric acid is associated with high blood pressure, metabolic syndrome, chronic kidney disease and cardiovascular disease. Whether lowering uric acid in people without gout protects the kidneys or heart is uncertain; two large trials (CKD-FIX and PERL) did not show that allopurinol slowed kidney disease. Current guidelines therefore do not recommend treating asymptomatic hyperuricemia with medication in most people.

Comparing uric acid targets across countries

Gout guidance from different regions expresses the same target in different units, which is a common source of confusion for patients who read international material:

The British Society for Rheumatology guideline is notable for recommending the lower target of 300 µmol/L (5 mg/dL) as standard. Whatever target your clinician chooses, the treat-to-target principle is the same: increase the dose until the level is consistently below the target, then continue long term.

When to see a doctor

See a doctor if you have sudden, severe pain, redness and swelling in a joint – classically the base of the big toe – especially with a raised uric acid; seek urgent care if you also have a fever, because a joint infection must be excluded. Discuss your result if your uric acid is above 9 mg/dL (535 µmol/L), if you have kidney stones, or if you have gout and your level stays above 6 mg/dL (360 µmol/L) despite treatment. Do not stop urate-lowering medicines during a flare unless advised; stopping often makes flares more frequent.