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Uric Acid

The end product of purine breakdown, cleared by the kidneys and gut. Raised levels can crystallise in joints as gout and track closely with metabolic health.

Curated · human-reviewed · Last reviewed

Typical adult reference range: 208 – 428 μmol/L
Ranges differ between laboratories, assays, sex and age. The range printed on your own report takes precedence over this one.

What is uric acid?

Uric acid is what is left when the body breaks down purines — the building blocks of DNA, RNA and the energy carrier ATP. Most of it comes from the turnover of the body's own cells, with a smaller share from purines in food. Humans run higher levels than almost every other mammal because we lost the enzyme uricase during evolution and cannot break uric acid down any further; it has to be excreted as is, about two-thirds through the kidneys and one-third through the gut. Blood levels therefore reflect a balance between how much is made and how much the kidneys let go, and in most people with high levels it is the second half of that balance — reduced excretion — that is off.

What is uric acid made of, and where does it come from?

Uric acid is a small heterocyclic molecule (168 daltons) made in the final two steps of purine catabolism by the enzyme xanthine oxidase, which turns hypoxanthine into xanthine and xanthine into uric acid. At blood pH it circulates almost entirely as the urate ion, and results are reported as serum urate in mg/dL or µmol/L (1 mg/dL = 59.5 µmol/L). Its solubility limit in body fluids at 37 °C is about 6.8 mg/dL (405 µmol/L); above that, monosodium urate can crystallise in joints and soft tissue, which is the physical basis of gout.

What does uric acid do in the body?

Uric acid is mainly a waste product, but not entirely. In plasma it is the single largest antioxidant, accounting for roughly half of the blood's free-radical scavenging capacity, which is one reason humans may have tolerated losing uricase. Inside cells and at high concentrations the picture reverses: urate promotes oxidative stress, inflammation and, in laboratory studies, insulin resistance and raised blood pressure. The kidney handles it in an elaborate way — nearly all filtered urate is reabsorbed by transporters such as URAT1 and GLUT9, then a portion is secreted again, so only about 10% of what is filtered leaves in the urine. Small genetic differences in these transporters explain much of why serum urate varies between people, more than diet does.

What does a high uric acid mean?

A raised serum urate (hyperuricaemia) means the body is holding more urate than it clears, and it raises the likelihood of three things without guaranteeing any of them. The best known is gout: urate crystals in a joint provoke intensely painful flares, yet only a minority of people with high urate ever develop gout, and the risk climbs with the level and the years spent above the solubility limit. The second is kidney involvement — uric acid kidney stones, and an association in cohort studies with faster loss of kidney function. The third is cardiometabolic: high urate clusters with obesity, insulin resistance, high blood pressure, fatty liver and raised triglycerides, and is a marker of that cluster as much as a cause. The 2020 ACR gout guideline recommends against starting urate-lowering medication for hyperuricaemia alone, without gout, which reflects how uncertain the benefit of lowering the number by itself remains.

Common causes:

  • Reduced kidney excretion, which accounts for roughly nine in ten cases — inherited variants in urate transporters (SLC2A9, ABCG2), insulin resistance, chronic kidney disease, and drugs such as thiazide and loop diuretics, low-dose aspirin and ciclosporin.
  • Increased production from diet — organ meats, shellfish, beer and spirits, and fructose-sweetened drinks.
  • Increased production from rapid cell turnover — psoriasis, blood cancers, chemotherapy (tumour lysis), haemolysis.
  • Metabolic states — obesity, metabolic syndrome, fasting or ketogenic diets, and dehydration.
  • Rare enzyme defects of purine metabolism, usually apparent from childhood.

What does a low uric acid mean?

A low serum urate is usually harmless and most laboratories do not flag it. It is expected in people taking urate-lowering medicines, in pregnancy, and on very low-purine or plant-based diets. Cohort studies have reported associations between low urate and Parkinson's disease and some other neurodegenerative conditions, consistent with its antioxidant role, but the direction of cause is unclear and no action follows from a low value on its own. A persistently very low level can occasionally point to a rare kidney tubular disorder or an inherited xanthine oxidase deficiency.

Common causes:

  • Urate-lowering therapy for gout, or other drugs with a uricosuric side effect — losartan, fenofibrate, SGLT2 inhibitors, high-dose aspirin, some calcium channel blockers.
  • Pregnancy, especially the first two trimesters, and oestrogen therapy.
  • A very low-purine, largely plant-based diet.
  • Rare: hereditary xanthinuria, Fanconi syndrome, syndrome of inappropriate antidiuretic hormone.

What moves uric acid apart from disease?

Purine-rich meals in the preceding day raises it
Organ meats, shellfish, anchovies, sardines and large portions of red meat raise serum urate within hours, and the Health Professionals Follow-up Study found that meat and seafood intake predicted new gout over 12 years while purine-rich vegetables did not. Diet moves the level by less than genetics does, but it is what moves it from one day to the next.
Alcohol and fructose raises it
Both work by the same route: their metabolism in the liver consumes ATP, and the purines released are converted to uric acid. Beer adds purines of its own and raises urate the most; spirits are next; wine in moderation has the weakest association. Sugar-sweetened soft drinks and fruit juice deliver fructose, and in prospective cohorts two or more servings a day roughly doubled the risk of gout.
Diuretics and low-dose aspirin raises it
Thiazide and loop diuretics reduce urate excretion by the kidney and are among the most common medication-related causes of a raised level. Aspirin is dose-dependent: the low doses used for heart protection retain urate, while high anti-inflammatory doses increase its excretion. Neither is a reason to stop a prescribed drug — it is a reason to read the result in context.
Fasting, ketosis and rapid weight loss raises it
Ketone bodies compete with urate for excretion in the kidney, so prolonged fasting, a ketogenic diet or the first weeks of aggressive weight loss push urate up and can trigger gout flares in people prone to them. Gradual weight loss lowers urate over the longer term.
Strenuous exercise and dehydration raises it
Exhaustive exercise breaks down ATP in muscle and releases purines, and the sweat loss concentrates the blood. Serum urate rises for a day or so after a marathon or a heavy session, and dehydration is one of the classic triggers of a gout flare.
Sex and hormonal status either direction
Oestrogen increases urate excretion, so premenopausal women run substantially lower than men of the same age and gout before the menopause is uncommon. Levels in women rise after the menopause and the gap narrows. Many laboratories therefore publish sex-specific reference intervals.

Which foods affect uric acid?

  • Low-fat dairy — milk, yoghurt — which increases urate excretion — lowers strong evidence
  • Coffee, regular or decaffeinated, in habitual drinkers — lowers moderate evidence
  • A DASH-style pattern rich in vegetables, fruit, whole grains and low-fat dairy — lowers moderate evidence
  • Cherries and tart cherry products — lowers emerging evidence
  • Organ meats, shellfish, anchovies, sardines and large red-meat portions — raises strong evidence
  • Beer and spirits — raises strong evidence
  • Sugar-sweetened soft drinks and fruit juice, through their fructose — raises strong evidence
  • Purine-rich vegetables such as spinach, mushrooms and legumes — despite the purines, not associated with gout — supports moderate evidence

Which supplements are studied for uric acid?

Vitamin C moderate evidence
Vitamin C increases urate excretion by the kidney. A meta-analysis of randomised trials found a modest average reduction of about 0.35 mg/dL (20 µmol/L) at around 500 mg a day in people without gout; a trial in people with established gout found the effect too small to matter clinically.
Typical dose: 500 mg/day, the dose used in most trials
Cautions: The effect is far too small to substitute for urate-lowering treatment in gout, and the 2020 ACR guideline does not recommend it for that purpose. Doses above about 1 g a day raise urinary oxalate and are associated with kidney stones, especially in people who have had them.
Tart cherry extract emerging evidence
Cherries contain anthocyanins with anti-inflammatory activity and a mild effect on urate. A case-crossover study found cherry intake in the preceding two days associated with fewer gout flares, and small short trials report modest urate reductions, but the products, doses and durations studied vary too much to state a standard dose.
Typical dose: no general dose given
Cautions: Juice and concentrate carry a substantial sugar load; fructose raises urate, which can offset the intended effect. Not a substitute for prescribed urate-lowering treatment in established gout.

How does exercise affect uric acid?

Regular moderate aerobic activity moderate evidence
How much: 150 minutes a week of moderate intensity — brisk walking, cycling, swimming — with attention to drinking enough during and after.
What to expect: Lowers urate over months mainly by reducing weight and insulin resistance rather than by any direct effect, and in cohorts is associated with fewer gout flares and lower mortality in people with gout.
Resistance training moderate evidence
How much: Two or three sessions a week at moderate load, avoiding exhaustive sessions when a flare is brewing.
What to expect: Improves insulin sensitivity and supports weight control, which lowers urate indirectly. Very heavy or exhaustive sessions raise urate for a day through ATP breakdown, so the benefit comes from the routine, not from any single hard workout.

Which lifestyle factors affect uric acid?

Gradual weight loss where relevant strong evidence
Weight loss lowers serum urate and reduces gout flares, and the 2020 ACR guideline conditionally recommends it for people with gout who are overweight. Gradual matters: crash diets and prolonged fasting raise urate through ketosis and can precipitate a flare.
Alcohol, especially beer and spirits strong evidence
Reducing alcohol is among the highest-yield changes for serum urate, and binge drinking is a well-documented flare trigger. The 2020 ACR guideline conditionally recommends limiting alcohol in gout regardless of disease activity.
Hydration moderate evidence
Adequate fluid intake dilutes urinary urate and lowers the risk of uric acid stones; dehydration concentrates serum urate and is a classic trigger of flares, particularly in hot weather and after exercise.
Medication review with the prescriber moderate evidence
Thiazide and loop diuretics, low-dose aspirin, ciclosporin and some tuberculosis drugs raise urate, while losartan and fenofibrate lower it. Where alternatives exist, the 2020 ACR guideline conditionally suggests switching — a decision for the prescribing clinician, not a reason to stop a drug independently.

How should you prepare for a uric acid test?

  • Fast overnight if the laboratory requests it, and avoid alcohol, organ meats and shellfish for 24 hours beforehand — each can raise the result on its own.
  • Avoid exhaustive exercise for 24 hours and drink normally; dehydration concentrates serum urate.
  • During a gout flare serum urate is often normal or even low, because inflammation increases its excretion. A value taken to assess gout is more informative two or more weeks after the flare has settled.
  • Mention diuretics, aspirin, and any recent start or stop of urate-lowering treatment, since each shifts the result.
  • Check the units. Reports use either mg/dL or µmol/L (1 mg/dL = 59.5 µmol/L), and the 6.8 mg/dL solubility threshold corresponds to about 405 µmol/L.
  • Day-to-day variation is meaningful; a single borderline value is worth repeating before conclusions are drawn.

References

  1. FitzGerald JD et al. 2020 American College of Rheumatology Guideline for the Management of Gout. Arthritis Care Res 2020 — https://doi.org/10.1002/acr.24180
  2. Dalbeth N, Gosling AL, Gaffo A, Abhishek A. Gout. Lancet 2021 — https://doi.org/10.1016/S0140-6736(21)00569-9
  3. Choi HK et al. Purine-Rich Foods, Dairy and Protein Intake, and the Risk of Gout in Men. N Engl J Med 2004 — https://doi.org/10.1056/NEJMoa035700
  4. Choi HK, Curhan G. Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. BMJ 2008 — https://doi.org/10.1136/bmj.39449.819271.BE
  5. Richette P et al. 2016 updated EULAR evidence-based recommendations for the management of gout. Ann Rheum Dis 2017 — https://doi.org/10.1136/annrheumdis-2016-209707

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Compiled from published medical literature and human-reviewed. For general health education only — it does not replace diagnosis or treatment advice from a doctor.