Lab result explainedMetabolic panelLast updated November 1, 2026

Uric acid blood test: what high and low levels mean and how to lower uric acid

Uric acid · Uric acid (serum urate) · reported in mg/dL (multiply by 59.5 for µmol/L)

Uric acid is the waste product your body makes when it breaks down purines, the building blocks of DNA found in every cell and in many foods, and a uric acid blood test measures how much is circulating. On most US reports the normal range is about 3.5 to 7.2 mg/dL for men and 2.5 to 6.0 mg/dL for women. The two most common reasons it is high are kidneys that excrete urate less efficiently (which runs in families and is worsened by diuretics, obesity and insulin resistance) and a diet high in fructose, alcohol and purine-rich meat and seafood.

Uric acid matters because above about 6.8 mg/dL it stops dissolving fully in body fluids and can crystallise in joints, causing gout, and in the urinary tract, causing kidney stones. Not everyone with a high level gets gout: around two-thirds of people with hyperuricemia never have an attack. But the higher and longer the elevation, the more likely crystals form, and a level of 9 mg/dL or more carries roughly a one-in-five annual chance of a first gout attack.

A low uric acid is uncommon and usually harmless. It is most often caused by urate-lowering medication, a low-purine or vegan diet, or pregnancy, and occasionally by inherited kidney tubule conditions. Both high and low readings are interpreted alongside kidney function, blood sugar and lipids, because uric acid tends to rise with the same metabolic problems that raise blood pressure and A1C.

Uric acid at a glance

What it is: the end product of purine breakdown, cleared mainly by the kidneys (about two-thirds) and the gut (one-third).
Normal: about 3.5–7.2 mg/dL in men, 2.5–6.0 mg/dL in women; hyperuricemia is usually defined as above 7.0 (men) or 6.0 (women).
High uric acid raises the risk of gout, kidney stones and is linked to high blood pressure, kidney disease and metabolic syndrome.
Crystals start forming above about 6.8 mg/dL; the treatment target in gout is below 6.0 mg/dL (below 5.0 with tophi).
Low uric acid (below 2.0 mg/dL) is usually due to medication, diet or pregnancy and rarely needs treatment.
Next step: repeat the test off alcohol and after a flare has settled, check creatinine, glucose and lipids, and address weight, sugary drinks and alcohol.

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What Uric acid measures

Purines from your own cell turnover (about two-thirds) and from food (about one-third) are broken down in the liver by the enzyme xanthine oxidase into uric acid. Humans lack the enzyme uricase that most mammals use to break uric acid down further, so levels in people run close to the solubility limit. About 70 percent of uric acid is removed by the kidneys and 30 percent by the gut; the kidneys filter it and then reabsorb about 90 percent through transporters such as URAT1, which is why most hyperuricemia is a problem of under-excretion rather than over-production.

The lab measures uric acid in serum using an enzymatic (uricase) colorimetric method. Results are reported in mg/dL in the US and µmol/L elsewhere (multiply mg/dL by 59.5). Levels are lower in children and premenopausal women because estrogen increases urate excretion, and rise after menopause to approach male values. Heavy exercise, dehydration, fasting and a recent large meat or alcohol meal all raise the reading for a day or two, so a borderline result is worth repeating under ordinary conditions.

Normal range for Uric acid

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

Group	Typical range (mg/dL (multiply by 59.5 for µmol/L))	Notes
Adult men	3.5–7.2 mg/dL	Some labs extend to 8.0. Above 7.0 is generally called hyperuricemia.
Adult women (premenopausal)	2.5–6.0 mg/dL	Above 6.0 is hyperuricemia. Estrogen increases urate excretion.
Women after menopause	Rises toward male values	Gout incidence in women climbs after 60 for this reason.
Children	About 2.0–5.5 mg/dL	Rises through puberty, earlier and higher in boys.
Saturation point	About 6.8 mg/dL	Above this, urate can crystallise in joints and tissues, especially in cooler peripheral joints like the big toe.
Gout treatment target	Below 6.0 mg/dL	Below 5.0 mg/dL for tophaceous or frequent gout (American College of Rheumatology 2020).
Very high	Above 9–10 mg/dL	Annual gout risk around 5 percent at 9 mg/dL and higher above; risk of urate kidney stones and, during chemotherapy, tumour lysis.
Low (hypouricemia)	Below 2.0 mg/dL	Usually from medication, diet or pregnancy; rarely an inherited kidney transporter defect.

High uric acid (hyperuricemia)

A high uric acid means more urate is being produced than the kidneys and gut are clearing. In roughly 90 percent of cases the main issue is under-excretion: inherited variants in urate transporters, reduced kidney function, diuretics or the insulin resistance that comes with excess weight all make the kidneys hold on to more urate. Over-production from a purine-heavy diet, alcohol, fructose, rapid cell turnover (psoriasis, blood cancers, chemotherapy) or rare enzyme defects adds to it.

On its own, a high level without symptoms (asymptomatic hyperuricemia) is not routinely treated with medication; the American College of Rheumatology advises against drug treatment unless gout, tophi, urate stones or very high levels during chemotherapy are present. It is, however, a useful warning: hyperuricemia is strongly associated with high blood pressure, fatty liver, type 2 diabetes and chronic kidney disease, and the lifestyle changes that lower it improve those too.

If you have had a painful, swollen joint, a high uric acid supports a diagnosis of gout but does not prove it. During an acute flare, the level can actually be normal in up to a third of people because inflammation increases urate excretion, so the test is best repeated two or more weeks after the attack settles. Finding urate crystals in joint fluid is the definitive test.

Common causes

Reduced kidney excretion (genetic and metabolic)
Variants in the URAT1, GLUT9 and ABCG2 transporters increase reabsorption of filtered urate, and insulin resistance has the same effect. This is the dominant cause of hyperuricemia and why gout clusters in families.
Obesity, metabolic syndrome and insulin resistance
High insulin levels tell the kidney to reabsorb more urate and visceral fat increases purine turnover. Each 5-unit rise in BMI raises gout risk substantially; weight loss lowers urate in proportion.
Diuretics and other medications
Thiazides and loop diuretics reduce urate excretion and are the most common drug cause. Low-dose aspirin, cyclosporine, tacrolimus, pyrazinamide, ethambutol, levodopa, niacin and testosterone also raise levels.
Fructose, sugary drinks and alcohol
Fructose metabolism consumes ATP and generates purines, and sugar-sweetened soft drinks roughly double gout risk at two or more a day. Beer supplies purines and alcohol of any kind raises lactate, which blocks urate excretion.
Purine-rich foods
Red meat, organ meats (liver, kidney), anchovies, sardines, shellfish and meat extracts raise serum urate and are associated with more gout flares. Purine-rich vegetables (spinach, lentils, mushrooms) do not increase risk.
Chronic kidney disease
As filtration falls, less urate is cleared; most people with an eGFR under 30 have hyperuricemia. High urate may in turn accelerate kidney damage, though trials of lowering it to protect the kidney have been disappointing.
Dehydration, fasting and ketogenic diets
Concentrated blood and ketones compete with urate for excretion, so crash diets, very low-carbohydrate diets and dehydration produce a temporary rise and can trigger a gout flare in the first weeks.
High cell turnover
Psoriasis, hemolytic anemia, leukemia, lymphoma, polycythemia and especially chemotherapy (tumour lysis) release large amounts of purines; levels can spike to over 15 mg/dL during tumour lysis.
Hypothyroidism, hyperparathyroidism and lead exposure
Each reduces kidney urate clearance. Lead nephropathy (saturnine gout) is rare today but still seen with moonshine and some imported ceramics.
Rare inherited enzyme defects
HGPRT deficiency (Lesch-Nyhan and partial variants) and PRPP synthetase overactivity cause massive over-production, gout in teenagers and uric acid stones.

Symptoms that can go with it

Usually none; most people with high uric acid feel nothing
Sudden, severe pain, swelling, heat and redness in one joint, classically the big toe, often starting at night (gout flare)
Attacks in the ankle, knee, wrist, finger or elbow, lasting days to two weeks
Firm chalky lumps under the skin of the ears, elbows, fingers or feet (tophi) after years of untreated gout
Severe pain in the side or back radiating to the groin, with blood in the urine (uric acid kidney stone)
Joint stiffness and damage between attacks in long-standing gout

Low uric acid (hypouricemia)

A uric acid below about 2.0 mg/dL is uncommon, found in fewer than 1 percent of blood tests, and most of the time it is a side effect of something expected: urate-lowering drugs such as allopurinol or febuxostat, a vegan or very low-purine diet, pregnancy, or the extra urate excretion that comes with SGLT2 inhibitors (diabetes and heart-failure drugs), losartan and fenofibrate.

The rare cases that matter are the inherited conditions in which the kidney tubule cannot reabsorb urate (renal hypouricemia, usually from URAT1 or GLUT9 variants), which can cause exercise-induced acute kidney injury and uric acid stones, and conditions such as Fanconi syndrome, Wilson disease or hereditary xanthinuria. Low uric acid is also sometimes seen in SIADH, liver failure and with very high-dose vitamin C. There is no evidence that a low level needs to be raised for its own sake.

Common causes

Urate-lowering medication
Allopurinol and febuxostat block xanthine oxidase; probenecid, lesinurad, losartan, fenofibrate and SGLT2 inhibitors increase urate excretion. A low level on treatment is expected and is not a problem.
Low-purine, vegetarian or vegan diet
Plant-based diets lower urate by about 0.5 to 1 mg/dL, partly from fewer purines and partly from the alkaline urine that aids excretion. Levels in the low-normal range on such diets are healthy.
Pregnancy
Increased kidney filtration and plasma volume lower urate in the first and second trimesters. A rising urate in the third trimester is one of the signs watched for in preeclampsia.
Inherited renal hypouricemia
Loss-of-function variants in URAT1 (SLC22A12) or GLUT9 (SLC2A9) mean the kidney cannot reabsorb urate. Usually harmless but linked to kidney stones and to acute kidney injury after intense exercise.
Fanconi syndrome and other tubule disorders
Generalised proximal tubule damage from drugs (tenofovir, ifosfamide), heavy metals, myeloma or inherited disease causes urate, phosphate, glucose and amino acids to leak into the urine together.
Liver disease, SIADH and Wilson disease
Severe liver failure reduces xanthine oxidase activity; SIADH dilutes the blood and increases urate clearance; Wilson disease damages the tubules through copper deposition.
Hereditary xanthinuria and high-dose vitamin C
Absent xanthine oxidase means purines stop at xanthine, which can form stones. Vitamin C at 1 to 2 g a day increases urate excretion modestly and can lower a borderline level.

Symptoms that can go with it

Almost always none
Flank pain or blood in the urine from xanthine or uric acid stones in the inherited conditions
Loin pain, nausea and reduced urine output within hours of intense exercise (exercise-induced kidney injury in renal hypouricemia)

Read it alongside

Creatinine and eGFR — reduced kidney function is both a cause of high urate and a reason to choose drug doses carefully.
A1C and fasting glucose — hyperuricemia travels with insulin resistance; a high urate is a prompt to screen for prediabetes.
Lipid panel and ALT — high triglycerides and fatty liver share the same fructose and insulin-resistance drivers.
Blood pressure — urate and hypertension rise together, and diuretic treatment for one worsens the other.
24-hour urine uric acid — separates over-producers (above 800 mg a day) from under-excreters, which guides drug choice and stone risk.
Joint fluid analysis — needle-shaped, negatively birefringent urate crystals are the definitive test for gout; the blood level is supporting evidence only.
CBC and TSH — rule out blood disorders and hypothyroidism as contributors.
Urine pH — acidic urine (pH below 5.5) favours uric acid stones even at modest serum levels.

What usually happens next

A borderline result is repeated after a normal week: no gout flare for at least two weeks, no alcohol binge, normal hydration and no unusual exercise.
Expect your clinician to check creatinine, glucose or A1C, lipids and blood pressure, since hyperuricemia is a metabolic marker as much as a gout marker.
If you have had a swollen joint, ask whether joint aspiration or an ultrasound (which shows the double-contour sign of urate on cartilage) can confirm gout.
Review your medications: a thiazide diuretic can sometimes be swapped for losartan or amlodipine, which lower urate instead of raising it.
If you have confirmed gout with two or more flares a year, tophi, stones or kidney disease, urate-lowering therapy (usually allopurinol, started low and titrated to a level below 6 mg/dL) is recommended and is far more effective than diet alone.
Ask whether you are a candidate for lifestyle-only management (asymptomatic, under 9 mg/dL, no gout) and what level would change that.

Diet, lifestyle and natural levers with evidence

What can move Uric acid once the cause is known. Nothing here replaces finding the cause.

Cut sugary drinks, fruit juice and beer

Strong evidence

In the Health Professionals Follow-up Study (46,000 men over 12 years), two or more sugar-sweetened soft drinks a day raised gout risk by 85 percent and beer raised it more than spirits or wine. Short-term feeding studies show fructose raises serum urate within hours. Removing these is the single most effective dietary change and usually lowers urate by around 0.5 to 1 mg/dL.

Diet soda does not raise urate. Whole fruit in normal amounts is fine; the problem is concentrated liquid fructose.

Weight loss

Moderate evidence

A systematic review found that losing about 7 to 10 kg lowered serum urate by roughly 0.3 to 1 mg/dL and reduced gout flares in most studies, with larger effects after bariatric surgery (often 2 mg/dL or more). The mechanism is lower insulin, which lets the kidney excrete more urate. Gradual loss is important because rapid weight loss and ketosis temporarily raise urate and can trigger a flare.

Avoid crash diets and prolonged fasting; aim for 0.5 to 1 kg a week.

DASH or Mediterranean-style eating pattern

Moderate evidence

In a randomised crossover trial of 103 adults with high blood pressure, the DASH diet (rich in fruit, vegetables, legumes, low-fat dairy and whole grains, low in red meat and sweets) lowered serum urate by 0.35 mg/dL overall and by about 1 mg/dL in those starting above 7 mg/dL, an effect comparable to a low dose of allopurinol in that subgroup. The pattern also lowers blood pressure and insulin resistance, which drive urate.

Low-fat dairy

Moderate evidence

Dairy proteins (casein and lactalbumin) increase urate excretion, and each daily serving of low-fat dairy was associated with a lower risk of gout in cohort studies. A randomised trial in people with gout found a skim-milk powder enriched with glycomacropeptide reduced flare frequency over three months, and acute studies show a glass of skim milk lowers serum urate within hours.

Full-fat dairy shows a weaker association; choose low-fat milk and yogurt.

Tart cherries

Preliminary evidence

An online case-crossover study of 633 people with gout found cherry intake over two days was associated with a 35 percent lower risk of a flare, and 75 percent lower when combined with allopurinol. Small trials of cherry juice or extract show modest urate reductions (around 0.2 to 0.5 mg/dL) and lower CRP, but no large randomised trial has confirmed a reduction in attacks.

Cherry juice concentrates are high in sugar; use tart cherry extract or limit to small amounts.

Vitamin C

Preliminary evidence

A meta-analysis of 13 randomised trials found about 500 mg of vitamin C a day lowered serum urate by 0.35 mg/dL on average, through increased kidney excretion. However, a trial in people with established gout found 500 mg a day made no clinically useful difference compared with allopurinol, so it is at best a minor add-on, not a treatment for gout.

Doses above 1 g a day can increase oxalate kidney stone risk in susceptible people.

When to see a clinician promptly

A hot, swollen, red joint with fever or feeling unwell: septic arthritis can look identical to gout and is an emergency; the joint should be aspirated the same day.
A first gout flare, or any flare lasting more than a few days despite anti-inflammatories, so the diagnosis can be confirmed and a long-term plan made.
Severe flank or back pain, nausea or blood in the urine, which may be a uric acid kidney stone.
Uric acid above 9 mg/dL, especially with kidney disease, diuretic use or a family history of gout, even without symptoms.
Two or more flares a year, tophi, or joint damage, which are indications for urate-lowering medication.
A very high level during chemotherapy or with a blood cancer, which can cause acute kidney injury (tumour lysis syndrome).

Frequently asked questions

Is a uric acid of 7.5 high?

Yes, mildly. It is above the 7.0 mg/dL threshold for hyperuricemia in men and well above the 6.0 limit for women, and above the 6.8 mg/dL saturation point where crystals can form. It does not mean you have gout; most people at this level never get an attack. It is a reason to look at weight, sugary drinks, alcohol and diuretics, repeat the test, and check kidney function and blood sugar.

What level of uric acid causes gout?

Risk rises steadily above 6.8 mg/dL, the point at which urate stops dissolving fully. In long-term studies the annual incidence of a first gout attack is about 0.5 percent at levels under 7, around 1 percent between 7 and 8.9, and around 5 percent at 9 mg/dL or more. The duration of elevation matters as much as the number; gout usually appears after years of hyperuricemia.

Does high uric acid always mean gout?

No. Roughly two-thirds of people with hyperuricemia never develop gout, and the American College of Rheumatology does not recommend medication for high uric acid alone. Conversely, uric acid can be normal during a gout flare because inflammation increases its excretion. Gout is diagnosed by symptoms, joint fluid crystals or ultrasound, with the blood level as supporting evidence.

Can dehydration raise uric acid?

Yes. Dehydration concentrates the blood and reduces urate excretion, so a sample taken after a hot day, heavy exercise, a night of drinking or a fast can read 0.5 to 1 mg/dL higher than your usual level. Repeat a borderline result when normally hydrated. Good fluid intake also reduces the risk of uric acid kidney stones, though it has only a small effect on serum levels in people who are not dehydrated.

How fast can diet lower uric acid?

Removing sugary drinks and beer and cutting back on red meat and shellfish typically lowers serum urate by 0.5 to 1 mg/dL within two to four weeks. Weight loss adds a further reduction over months. Diet alone rarely achieves more than a 1 to 1.5 mg/dL drop, which is why someone starting at 9 or 10 with established gout usually needs medication to reach the target of under 6.

Does coffee lower uric acid?

Regular coffee drinkers have lower uric acid and lower gout risk in large cohort studies: four or more cups a day was associated with about 40 percent lower gout risk in men. The effect appears in decaffeinated coffee too, suggesting chlorogenic acids rather than caffeine, possibly through improved insulin sensitivity. Trials are lacking, so it is a reasonable habit to keep rather than a treatment to start.

Is low uric acid dangerous?

Usually not. A low level is most often from urate-lowering medication, a plant-based diet or pregnancy and needs no action. The exception is inherited renal hypouricemia (levels often under 1 mg/dL), which can cause kidney stones and, rarely, acute kidney injury after strenuous exercise. Very low levels have been linked in observational studies to some neurological diseases, but there is no evidence that raising uric acid helps.

Do I need to fast before a uric acid test?

Most labs do not require it, but many clinicians prefer a fasting morning sample, and avoiding alcohol and a large meat meal for 24 hours beforehand gives a more representative result. Do not test during or within two weeks of a gout flare, and mention any diuretics, aspirin or vitamin C you take.

References

FitzGerald JD, Dalbeth N, Mikuls T, et al.. 2020 American College of Rheumatology guideline for the management of gout. Arthritis Care & Research (2020)
Uric acid test. MedlinePlus, US National Library of Medicine (2023)View source
High uric acid level: causes. Mayo Clinic (2024)View source
Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G. Purine-rich foods, dairy and protein intake, and the risk of gout in men. New England Journal of Medicine (2004)
Choi HK, Curhan G. Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. BMJ (2008)
Juraschek SP, Gelber AC, Choi HK, Appel LJ, Miller ER. Effects of the Dietary Approaches to Stop Hypertension (DASH) diet and sodium intake on serum uric acid. Arthritis & Rheumatology (2016)
Zhang Y, Neogi T, Chen C, Chaisson C, Hunter DJ, Choi HK. Cherry consumption and decreased risk of recurrent gout attacks. Arthritis & Rheumatism (2012)
Juraschek SP, Miller ER, Gelber AC. Effect of oral vitamin C supplementation on serum uric acid: a meta-analysis of randomized controlled trials. Arthritis Care & Research (2011)
Dalbeth N, Ames R, Gamble GD, et al.. Effects of skim milk powder enriched with glycomacropeptide and G600 milk fat extract on frequency of gout flares: a proof-of-concept randomised controlled trial. Annals of the Rheumatic Diseases (2012)
Hainer BL, Matheson E, Wilkes RT. Diagnosis, treatment, and prevention of gout. American Family Physician (2014)
Gout. Merck Manual Professional Version (2024)
Gout and kidney disease. National Kidney Foundation (2023)View source

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This page is educational and is not medical advice or a diagnosis. Lab results have to be interpreted together with your history, symptoms and other results by a clinician who knows you. Do not start or stop a supplement to change a lab value before the cause is known.