What the uric acid test shows
Uric acid is the final product of purine metabolism — purines come from the turnover of your own cells (their DNA and RNA) and from food. Humans lack the enzyme uricase, so uric acid cannot be broken down further, only excreted, mostly by the kidneys. A uric acid blood test measures how much is dissolved in your serum.
It differs from the kidney markers beside it. Creatinine and urea rise mainly when filtration fails; uric acid reflects both how much your body makes and how well the kidneys excrete it, so it can climb even when filtration is normal.
Uric acid normal range
Uric acid is reported in mg/dL in the US and µmol/L elsewhere (1 mg/dL ≈ 59.5 µmol/L). Men run higher than women because estrogen aids urate excretion, so women’s levels rise after menopause.
| Group | Conventional, mg/dL | SI, µmol/L |
|---|---|---|
| Men (adult) | ~3.4–7.0 | ~200–420 |
| Women (adult, premenopausal) | ~2.4–6.0 | ~140–360 |
| Women (postmenopausal) | approaches male range | approaches male range |
| Children / under 18 | lower; ~5.5 cutoff | lower; ~330 cutoff |
Two thresholds matter more than the “normal” band. Hyperuricemia is usually defined as above 6.8 mg/dL (about 400 µmol/L) — the point where urate stops staying dissolved and can crystallize into joints as gout or into uric acid stones — or by sex-specific cutoffs near 7.0 mg/dL (men) and 6.0 mg/dL (women). Once gout is present, the target is lower, below 6 mg/dL (360 µmol/L). Ranges depend on the lab, sex and age, so read your result against your own report.
Why uric acid is high
High uric acid (hyperuricemia) is the clinically important direction and the reason most people are tested. It reflects making too much urate, clearing too little, or both — and under-excretion is by far the commonest, per StatPearls. Roughly by frequency:
- Reduced kidney excretion (most cases): chronic kidney disease, dehydration and, very often, medicines — diuretics, low-dose aspirin, ciclosporin, tacrolimus. This is why creatinine is checked alongside.
- Insulin resistance and metabolic syndrome: high insulin makes the kidney retain urate, so hyperuricemia travels with obesity, type 2 diabetes, high blood pressure and fatty liver — part of the check-up in men over 30.
- Diet and alcohol: red meat, organ meats, shellfish, beer and fructose-sweetened drinks; alcohol also blocks excretion.
- High cell turnover: psoriasis, hemolysis and the tumor lysis after chemotherapy for leukemia or lymphoma.
- Rarer: inherited enzyme defects, hypothyroidism, lead.
Consequences include gout flares (classically the big toe), uric acid kidney stones, and links to hypertension, chronic kidney disease and cardiovascular disease.
When is it urgent? Tumor lysis syndrome — a rapid urate spike during cancer treatment that can cause kidney failure — is a medical emergency. A first hot, swollen, painful joint also needs prompt assessment to exclude septic arthritis; CRP helps flag it.
Why uric acid is low
Low uric acid (hypouricemia, usually below about 2 mg/dL / 120 µmol/L) is much less common and usually harmless — often just a medication effect. Causes include:
- Drugs that boost excretion or block production: urate-lowering therapy itself (allopurinol, febuxostat), uricosurics such as probenecid, losartan, high-dose vitamin C and SGLT2 inhibitors.
- Increased renal loss: Fanconi syndrome and inherited renal hypouricemia, which can paradoxically cause exercise-induced kidney injury and stones.
- Reduced production: advanced liver disease (the liver makes uric acid) and the rare disorder xanthinuria.
- Dilution: SIADH; normal pregnancy also lowers urate.
A low value alone rarely needs action, but if very low or unexplained it can point to liver disease or a kidney-handling problem worth checking.
What to test alongside
Uric acid is read next to kidney, metabolic and inflammation markers, not on its own:
- Creatinine — kidney filtration; urate’s main exit route.
- Urea — a second kidney marker, paired with creatinine.
- Glucose and HbA1c — the insulin resistance that drives high urate.
- Total cholesterol and LDL cholesterol — the same metabolic and cardiovascular-risk cluster.
- CRP — inflammation; rises in a flare and separates gout from joint infection.
- GGT, ALT and AST — liver and alcohol markers, since alcohol and fatty liver push urate up.
What to do about an abnormal result
- Don’t self-treat. Do not start allopurinol, high-dose vitamin C or a crash “purine detox” on your own — a high number with no symptoms often needs no drug.
- Repeat in context. Urate swings with dehydration, alcohol, a big meal and acute illness (it can even dip during a flare), so recheck an abnormal value when you are well and hydrated.
- High urate with gout or stones: a doctor or rheumatologist confirms the diagnosis and, if urate-lowering therapy is indicated, titrates it below 6 mg/dL (360 µmol/L) — the treat-to-target goal shared by the ACR and NICE, with NICE advising a tighter target under 5 mg/dL (300 µmol/L) for severe or tophaceous gout.
- High urate with no symptoms: guidelines conditionally advise against routine drug treatment; the priority is the drivers — weight, alcohol, diuretics, blood pressure and blood sugar.
- Low urate: usually no treatment; your doctor reviews medicines and, if very low or unexplained, checks liver function and sodium.
- See your GP first. They decide on any referral — rheumatology for gout, nephrology or urology for stones and kidney disease.
Mini-FAQ
What is a normal uric acid level?
Roughly 3.4–7.0 mg/dL (200–420 µmol/L) in men and 2.4–6.0 mg/dL (140–360 µmol/L) in women, and women’s levels rise after menopause. Hyperuricemia usually means a value above about 6.8 mg/dL (400 µmol/L), where urate starts to crystallize. Ranges vary by lab.
Does high uric acid always mean gout?
No. Most people with high uric acid never develop gout, and you can have a gout flare while the blood level looks normal. Gout is diagnosed from symptoms and, ideally, urate crystals in the joint — not from the number alone.
What causes high uric acid?
Most often the kidneys clearing too little — from chronic kidney disease, dehydration, diuretics or insulin resistance — plus a diet high in red meat, shellfish, beer and sugary drinks. Rapid cell turnover, as in cancer treatment, can cause sharp rises.
How can I lower my uric acid?
Treat the drivers: lose excess weight gradually, cut alcohol (especially beer) and fructose-sweetened drinks, stay hydrated, and review medicines such as diuretics with your doctor. If you have gout, your doctor may prescribe urate-lowering therapy aimed below 6 mg/dL — do not start it on your own.
Is low uric acid dangerous?
Usually not. It is often a side effect of medication and rarely needs treatment, though a very low or unexplained level can point to liver disease or a kidney-handling problem worth checking.
Should I treat high uric acid if I have no symptoms?
Major guidelines advise against routinely using urate-lowering drugs for asymptomatic hyperuricemia. The focus is on lifestyle and on managing linked conditions such as high blood pressure, diabetes and kidney disease.
