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Longevity Library · Lab reference

Written by Daniel Tagge, MD
Updated October 10, 2026
Reviewed October 10, 2026
27 sources · Measured in mg/dL

System: Metabolism & Metabolomics

Uric acidSerum urate

Urate causes gout, and the risk climbs steeply across the laboratory range: about 1 percent over 15 years below 6 mg/dL, 2.7 times that between 6 and 6.9, and about half of people above 10, which is why the gout guideline target is below 6. Higher urate also tracks with heart disease, kidney disease and death in cohorts, but genetic studies and three randomized trials of urate lowering found no causal effect on those outcomes, so outside gout and stones the number is best read as a marker of insulin resistance, fructose, alcohol, body weight, diuretics and kidney function.

Uric acid is the end product of purine breakdown, cleared mostly by the kidney, which reabsorbs most of what it filters. Laboratories print upper limits near the point at which urate crystallizes, about 6.8 to 7 mg/dL, lower in women because estrogen helps the kidney excrete it. The evidence is firm that urate causes gout and that lowering it treats gout, cautious about very low values, and clear that the heart and kidney associations have not survived genetic analysis or randomized trials.

01 · The scale

Where the laboratory range and the evidence sit.

Gout risk sat lowest below 6 mg/dL (about 1 percent over 15 years) and rose 2.7-fold at 6 to 6.9, 6.6-fold at 7 to 7.9 and 64-fold at 10 or more; above about 9 the cohorts recorded a new case in about 5 percent of men a year. Higher urate also tracked with heart disease, kidney disease and death in cohorts, but genetic studies found no causal effect and three randomized trials of urate lowering did not slow kidney decline. Very low urate, below about 3.5 in men and 2.5 in women, carried higher mortality in one large cohort.

024681012

  1. Common laboratory reference range (women)

    2.5 to 6 mg/dL · Typical US laboratories

  2. Common laboratory reference range (men)

    3.5 to 7.2 mg/dL · Typical US laboratories

  3. Very low urate: higher mortality in one Korean cohort (below 3.5 in men, 2.5 in women)

    0 to 3.5 mg/dL · Cho 2018

  4. 15-year gout incidence about 1 percent; the gout treatment target

    3.5 to 6 mg/dL · Dalbeth 2018; ACR 2020

  5. Gout hazard 2.7 times the band below; still under the saturation point

    6 to 6.8 mg/dL · Dalbeth 2018; ACR 2020

  6. Above the saturation point: gout hazard 6.6 to 15 times; about 0.5 percent a year in men

    6.8 to 9 mg/dL · ACR 2020; Dalbeth 2018; Campion 1987

  7. Gout in about 5 percent of men a year; hazard 30 to 64 times

    9 and above mg/dL · Campion 1987; Dalbeth 2018

  • Laboratory range
  • Evidence supports
  • Guideline goal or unstudied
  • Higher risk in studies
Scale in mg/dL. Some reports print µmol/L; multiply mg/dL by about 59.5. Bands show where studies found something, not a recommendation for any one person.

02 · What it is

What Uric acid measures.

Uric acid is what humans are left with when purines, the building blocks of DNA and of the energy molecule ATP, are broken down. The kidney excretes about two thirds of it and the gut the rest; the kidney filters urate freely and then reabsorbs most of it in the proximal tubule, so that 10 percent or less of what is filtered leaves in the urine. People eating traditional non-Western diets run about 2 to 4 mg/dL; industrialized populations run about 3 to 8, reflecting diets richer in purines and fructose, more alcohol, and more insulin resistance, hypertension and reduced kidney function, all of which cut the kidney's urate excretion.1Grade A

Urate is a cause of gout, of kidney stones and of the acute kidney injury that follows massive cell breakdown in tumor lysis syndrome. In the US national survey of 2015 to 2016, 3.9 percent of adults (9.2 million people) had gout, 5.2 percent of men and 2.7 percent of women; mean urate was 6.0 mg/dL in men and 4.8 in women, and about 20 percent of each sex had hyperuricemia, defined there as above 7.0 in men and 5.7 in women. Only a third of people with gout were on urate-lowering treatment.1,2Grade A

Urate rises with insulin resistance because insulin makes the kidney hold on to it. In 36 healthy volunteers, insulin resistance measured directly correlated with serum urate (r = 0.69) and inversely with urinary urate clearance, independent of age, sex and obesity. Genetic analysis settled the direction: genetically higher fasting insulin raised urate by about 0.37 mg/dL per log unit (0.69 after adjustment for body mass index), while genetically higher urate did not raise insulin. Insulin resistance drives urate, not the other way round.3,4Grade B

03 · The laboratory range

What a laboratory calls normal.

Up to about 7.0 to 8.0 mg/dL in men and about 6.0 to 7.0 in women, with lower limits near 2.5 to 3.5, depending on the laboratory.

The upper limit is set by chemistry as much as by statistics. Monosodium urate approaches its solubility limit in water at about 7 mg/dL, which is why the National Kidney Foundation workshop defines hyperuricemia as above 7 in men and above 6 in women, and why the American College of Rheumatology defines asymptomatic hyperuricemia as a urate of 6.8 mg/dL or more with no prior flare or tophus. Urate is more soluble in plasma than in water, so concentrations above 10 can occur without crystals forming. Women run lower before menopause because estrogen increases urate excretion by the kidney; after menopause their values approach men's.1,5Grade A

A laboratory range is a description of the population tested, not a verdict on risk. About one US adult in five exceeds the survey thresholds, and the pooled cohort data show gout risk already 2.7 times higher at 6.0 to 6.9 mg/dL than below 6, a band most laboratories print as normal. The number is best read against the gout curve and the person's own trend rather than against the flag.2,6Grade B

04 · The evidence

What the studies support.

The Normative Aging Study followed 2,046 initially healthy men for 14.9 years. With a prior urate of 9 mg/dL or more, the annual incidence of a first gout attack was 4.9 percent, against 0.5 percent at 7.0 to 8.9 and 0.1 percent below 7.0; above 9 the cumulative incidence reached 22 percent after five years. Once urate entered the model, age, body mass index, blood pressure, cholesterol and alcohol lost their independent predictive power, and the authors found no kidney deterioration attributable to hyperuricemia, which led them to recommend conservative management of asymptomatic hyperuricemia.7Grade B

Pooling individual data from 18,889 gout-free participants in four US cohorts (ARIC, CARDIA and both Framingham cohorts) followed for a mean of 11.2 years, the 15-year cumulative incidence of clinically evident gout ran from 1.1 percent below 6 mg/dL to 49 percent at 10 or more. Against below 6, the adjusted hazard was 2.7 times at 6.0 to 6.9, 6.6 at 7.0 to 7.9, 15 at 8.0 to 8.9, 30 at 9.0 to 9.9 and 64 at 10 or more. Even so, only about half of those above 10 developed gout over 15 years, so duration of exposure and other factors matter too.6Grade B

For people who have gout, the 2020 American College of Rheumatology guideline strongly recommends treating to a serum urate below 6 mg/dL, with the dose adjusted against serial measurements. For people with asymptomatic hyperuricemia it conditionally recommends against starting any urate-lowering drug: in the trials available, gout developed in under 1 percent of treated and 5 percent of untreated participants over 3 years, so 24 people would need treatment for 3 years to prevent one first flare, and the panel judged that the benefit does not outweigh cost and risk for the many who would never progress, including those with kidney disease, heart disease, stones or hypertension. After a first flare, a urate above 9, stage 3 or worse kidney disease, or kidney stones tips the guideline toward starting treatment.5Grade A

In cohorts, higher urate keeps company with heart disease and death. Across 26 prospective studies of 402,997 adults, hyperuricemia carried 1.09 times the adjusted risk of coronary heart disease and 1.16 times the coronary mortality, 1.12 per mg/dL, with the mortality signal confined to women (1.67). Across 11 prospective studies of 172,123 people, the highest urate category carried 1.24 times the all-cause and 1.37 times the cardiovascular mortality of the lowest. An umbrella review of 136 outcomes rated none of the observational associations convincing; five were highly suggestive (heart failure, hypertension, impaired fasting glucose or diabetes, chronic kidney disease, and coronary mortality), and 55 percent of the meta-analyses showed small-study effects or excess significance.8,9,10Grade A

Genetics do not support a causal role for urate in those outcomes. Using 14 variants that act only on urate, a one standard deviation genetic increase was not associated with type 2 diabetes (26,488 cases), coronary disease (54,501), ischemic stroke (14,779) or heart failure (4,526), while the same instrument raised gout odds 5.84-fold. For the kidney, Mendelian randomization in more than 400,000 people found no causal effect of urate on estimated GFR or chronic kidney disease, with more than 99 percent power to detect the observed association (1.99 mL/min lower eGFR and 1.48 times the odds of CKD per mg/dL), while gout odds rose 3.4- to 6.0-fold per mg/dL. The National Kidney Foundation workshop reached the same reading: cell and animal work and epidemiology point one way, Mendelian randomization generally does not.11,12,1Grade B

Three randomized trials then tested urate lowering in the kidney and found nothing. FEATHER randomized 467 Japanese adults with stage 3 kidney disease and asymptomatic hyperuricemia to a xanthine oxidase inhibitor or placebo for 108 weeks: the eGFR slope was 0.23 versus -0.47 mL/min per year (difference 0.70, confidence interval -0.21 to 1.62, P = 0.1), though gout fell from 5.86 to 0.91 percent. CKD-FIX randomized 369 adults with stage 3 or 4 kidney disease at high risk of progression and a mean urate of 8.2 mg/dL to urate-lowering treatment or placebo for 104 weeks: eGFR fell 3.33 versus 3.23 mL/min per year (P = 0.85). PERL randomized 530 adults with type 1 diabetes and early kidney disease for 3 years: urate fell from 6.1 to 3.9 mg/dL on treatment and stayed at 6.1 on placebo, measured GFR did not differ (0.001 mL/min), and albumin excretion ended 40 percent higher in the treated group.13,14,15Grade A

Kidney stones are the one outcome besides gout where lowering urate has helped in a trial, and even there the serum level is not the whole story. The umbrella review found that the only trial outcome meeting its strictest bar was fewer recurrent stones with urate-lowering treatment, and the gout guideline cites a trial in calcium oxalate stone formers with high urinary urate. But in the UK Biobank (359,827 people, 6,398 with stones), serum urate's association with stones vanished after adjustment (odds ratio 1.03) and genetically higher serum urate did not raise stone risk (0.93), so the serum number is a weaker guide than urine chemistry.10,5,16Grade B

Very low urate may not be benign. In 375,163 South Korean adults with 2,020 deaths over about 2 million person-years, mortality was U-shaped: against the sex-specific reference band, men below 3.5 mg/dL had 1.58 times and women below 2.5 had 1.80 times the all-cause mortality, while men at 9.5 or more had 2.39 times and women at 8.5 or more 3.77 times. A single cohort with few deaths at the extremes, and the earlier meta-analysis called the low end inconclusive; circulating urate reacts with oxidants, and a low value can also reflect illness, so this is a flag, not a finding.17,9,1Grade C

05 · What moves it

The levers with evidence behind them.

What is listed here has been tested. The size of each effect, and the size of the study, are in the sentence, so a small effect reads as a small effect.

  • Sugar-sweetened drinks and fructose

    raise it; two or more sodas a day about doubled gout risk

    In 46,393 men followed 12 years, two or more sugar-sweetened soft drinks a day carried 1.85 times the gout risk of under one a month, and the top fifth of fructose intake 2.02 times; diet soda carried none. In 78,906 women followed 22 years, two or more sodas a day carried 2.39 times the risk and two or more orange juices 2.42 times, though the absolute excess was small, 68 and 47 extra cases per 100,000 person-years. A gram of fructose per kilogram of body weight raises urate by 1 to 2 mg/dL within two hours, which is why the gout guideline conditionally recommends limiting high-fructose corn syrup.18,19,5Grade B

  • Alcohol, beer and spirits more than wine

    raises it; abstaining ran about 1.6 mg/dL lower

    In 47,150 men followed 12 years, gout risk rose with alcohol in a dose-response fashion, 1.49 times at 15 to 29.9 grams a day and 2.53 times at 50 or more; each daily beer carried 1.49 times the risk and each daily shot 1.15, while wine carried none (1.04). People with gout who limited or abstained ran 1.6 mg/dL lower than those who did not, and a unit of beer raised urate by about 0.16 mg/dL in a diet-and-genetics analysis, which found the effect of any single food small next to genetics.20,5Grade B

  • Meat and seafood up, dairy down

    modest; purine-rich vegetables and total protein did not matter

    In the same 47,150 men, the highest fifth of meat intake carried 1.41 times the gout risk and of seafood 1.51 times, while the highest fifth of dairy intake carried 0.56 times; purine-rich vegetables and total protein carried no excess. The effect of diet on the number itself is small: a trial of low-purine education in people already at target did not lower urate, and the guideline rates its purine-limiting recommendation as low-certainty.21,5Grade B

  • Weight loss

    lowers it, by about 1 mg/dL per 5 kg in small studies

    Across 10 longitudinal studies (one randomized) of overweight people with gout, mean weight losses of 3 to 34 kg changed urate by -168 to +30 µmol/L (about -2.8 to +0.5 mg/dL), and 0 to 60 percent reached the target below 360 µmol/L (6 mg/dL); six of eight studies reduced attacks, with a temporary rise in urate and flares after bariatric surgery. In the guideline's review, a 5 kg loss lowered urate 1.1 mg/dL in 11 obese patients and a 34.3 kg loss after bariatric surgery lowered it 2.0 mg/dL, and a body mass index fall of more than 5 percent carried 40 percent lower odds of a recurrent flare.22,5Grade B

  • Insulin resistance

    raises it by reducing kidney excretion

    Because insulin makes the kidney reabsorb urate, the metabolic syndrome travels with a higher urate: insulin resistance correlated with urate at r = 0.69 in healthy volunteers, and genetically higher fasting insulin raised urate (0.37 to 0.69 mg/dL per log unit) while genetically higher urate did not change insulin. Reducing insulin resistance lowers urate; lowering urate with a drug is not expected to improve insulin resistance.3,4Grade B

  • Diuretics and other medications

    diuretics raise it by about 0.7 mg/dL and raise gout risk

    In 5,789 adults with hypertension in the ARIC cohort, starting a diuretic raised urate by 0.72 mg/dL more than not starting one, and diuretic use carried 1.48 times the gout risk (thiazides 1.44, loop diuretics 2.31), an effect fully explained by the urate change; other blood-pressure drugs carried 0.64 times the risk. The gout guideline conditionally recommends switching a thiazide to an alternative when feasible and preferring the one angiotensin receptor blocker that lowers urate, but only when the prescriber judges the benefit worth the change; it recommends against stopping low-dose aspirin taken for a good reason.23,5Grade B

  • A DASH-style eating pattern

    lowers it by about 0.25 mg/dL

    Pooling four randomized trials with 590 participants, a DASH diet for at least four weeks lowered urate by 0.25 mg/dL with no heterogeneity. Six trials of ketogenic diets in 267 people showed no consistent change (pooled +0.26 mg/dL, confidence interval -0.47 to +0.98, heterogeneity 95 percent), which means individual responses ran in both directions.24Grade B

  • Hard exercise

    raises it for a day or more after intense effort; steady effort does not

    In untrained young men, repeated one-minute sprints at 120 percent of maximal oxygen uptake raised plasma urate 40 percent during the session, and the next morning's resting value was still elevated (476 versus 352 µmol/L, about 8.0 versus 5.9 mg/dL). Two hours of steady cycling at 65 percent of maximum did not raise it. Intensity, not total work, drives the rise, because fast-twitch fibers break down purine nucleotides under high energy demand.25Grade C

06 · Reading it well

Caveats, and what belongs with a physician.

Urate varies from week to week. The standing biological-variation database puts within-person variation at about 8.6 percent and between-person variation at 17.5 percent, so a change of a few tenths of a milligram is noise, and a single value near a threshold deserves a repeat before it is acted on. The European biological variation study found that within-person variation differs between men and women for urate, so the margins are not identical for the two sexes.26,27Grade C

Kidney function moves the number before any disease does. Two thirds of urate leaves through the kidney, and the workshop report notes that even subtle changes in kidney function alter serum urate; in the population cohorts, each 1 mg/dL of urate went with 1.99 mL/min lower estimated GFR. A rising urate therefore deserves a creatinine and eGFR beside it, and part of the cohort association with kidney disease is the kidney raising the urate rather than the urate harming the kidney.1,12Grade B

Timing matters. A sample drawn the morning after a hard interval or sprint session can read about 2 mg/dL higher than the person's baseline, and ketogenic or very-low-calorie eating has moved urate in both directions across trials. Diuretics add about 0.7 mg/dL. Read a surprising value against the previous day's activity, fluids, diet and medication list before reading it as a trend.25,24,23Grade C

Sex and life stage set the baseline. Estrogen increases urate excretion, so women run lower before menopause and approach men's values afterward; US means are 6.0 mg/dL in men and 4.8 in women, and the survey definition of hyperuricemia is correspondingly different (above 7.0 and above 5.7). A value that is unremarkable in a man can be the top of the distribution in a premenopausal woman.1,2Grade B

The cohort associations with heart disease, hypertension, diabetes and kidney disease are real as statistics and have not held up as causes: the umbrella review rated none convincing, Mendelian randomization found no causal effect on diabetes, coronary disease, stroke, heart failure or kidney function, and the kidney trials were null. Urate marks the insulin resistance, fructose, alcohol, weight, diuretic use and reduced kidney function that do the harm. Lowering the number with a drug has treated gout and nothing else so far.10,11,12,14,1Grade A

Asymptomatic hyperuricemia is, by guideline, a reason to look at causes and not a reason to start a urate-lowering drug: 24 people would need three years of treatment to prevent one first flare, and in the Normative Aging Study most men above 9 mg/dL had not developed gout after five years. The exceptions are spelled out in the guideline and belong with a physician: a flare, tophi, kidney stones, or a urate above 9 with kidney disease.5,7Grade A

See a physician

  • A hot, swollen, intensely painful joint, especially the base of the big toe, the ankle or the knee, whatever the urate reads; a first gout flare should be diagnosed, not assumed, and infection ruled out.
  • A kidney stone, blood in the urine or flank pain alongside a raised urate; urine chemistry, not the serum number, guides what to do.
  • A urate above about 9 mg/dL on repeat, the band in which about 5 percent of men a year developed gout in the cohorts and the guideline begins to weigh treatment after a first flare.
  • Any urate-lowering medication already in use: the dose is adjusted against serial measurements to a target below 6 mg/dL, and stopping or changing it is a decision for the prescriber.
  • A raised urate together with a falling estimated GFR, a new diuretic, or a very low urate below about 3 mg/dL without an obvious reason.

This page is education, not individual medical advice, and reading it creates no physician-patient relationship.

07 · Open questions

What the literature does not settle.

  • No trial has treated people without gout to a urate target and measured heart, kidney or mortality outcomes with benefit; the three kidney trials were null, and a cardiovascular outcome trial of urate lowering in asymptomatic people has not been done.
  • Why urate tracks so strongly with heart disease and death in cohorts when genetics find no causal effect is unresolved; candidate explanations are kidney function, insulin resistance, diuretics and the cell turnover of illness.
  • Whether urate crystal deposits seen on imaging in people who have never had a flare should change management is unsettled; the guideline treats them as asymptomatic.
  • The U-shaped mortality curve rests mainly on one Korean cohort; whether a very low urate is a cause of harm or a marker of illness, and whether there is a floor worth watching, is unknown.
  • Whether serum urate causes kidney stones, as the National Kidney Foundation states, or only urinary urate does, as the UK Biobank genetic analysis suggests, has not been reconciled.
  • Reference ranges are sex-specific but not stage-specific; no body has published an outcome-based range for premenopausal and postmenopausal women separately.

08 · In practice

How Dr. Tagge reads it in his own practice.

I like to see uric acid under 6 mg/dL in men and women alike. That is my judgment, and here is the reasoning: 6 is the target the gout guideline treats to, it is the line below which the pooled cohorts put 15-year gout risk at about 1 percent, and it keeps a margin under the 6.8 saturation point where crystals begin. Above 6 in someone who has never had a flare, I do not reach for a urate-lowering drug; the kidney trials and the genetics talked me out of that. I read the number as a report on insulin, fructose, alcohol, weight, diuretics and the kidney, and I work on those, which brings urate down as a side effect. A very low value gets a second look too.

A practice judgment, labeled as one (Grade D): it is how one physician reads the number for the people he cares for, not a recommendation for you.

09

Questions

10 · Sources

27 sources, read in full.

Numbered in the order they appear. Each line says what this page relies on from the paper; the link opens the record at PubMed or the publisher.

  1. 1.

    Johnson RJ, Bakris GL, Borghi C, et al.. Hyperuricemia, Acute and Chronic Kidney Disease, Hypertension, and Cardiovascular Disease: Report of a Scientific Workshop Organized by the National Kidney Foundation. American Journal of Kidney Diseases. 2018. PMID 29496260. DOI 10.1053/j.ajkd.2017.12.009.

    Consensus statement · Urate is a cause of gout, kidney stones and tumor lysis kidney injury; two thirds excreted by the kidney with fractional excretion of 10 percent or less; 7 mg/dL nearly matches solubility in water; estrogen lowers urate before menopause; Mendelian randomization generally does not support a causal role in kidney disease, hypertension or diabetes.

  2. 2.

    Chen-Xu M, Yokose C, Rai SK, Pillinger MH, Choi HK. Contemporary Prevalence of Gout and Hyperuricemia in the United States and Decadal Trends: The National Health and Nutrition Examination Survey, 2007-2016. Arthritis & Rheumatology. 2019. PMID 30618180. DOI 10.1002/art.40807.

    Cross-sectional study · Gout prevalence 3.9 percent (5.2 men, 2.7 women); mean urate 6.0 mg/dL in men and 4.8 in women; hyperuricemia (above 7.0 men, 5.7 women) in 20.2 and 20.0 percent; one third of gout patients on urate-lowering therapy.

  3. 3.

    Facchini F, Chen YD, Hollenbeck CB, Reaven GM. Relationship between resistance to insulin-mediated glucose uptake, urinary uric acid clearance, and plasma uric acid concentration. JAMA. 1991. PMID 1820474.

    Cross-sectional study · In 36 healthy volunteers, insulin resistance correlated with serum urate (r = 0.69) and inversely with urinary urate clearance (r = -0.49); the effect is exerted at the kidney.

  4. 4.

    McCormick N, O'Connor MJ, Yokose C, et al.. Assessing the Causal Relationships Between Insulin Resistance and Hyperuricemia and Gout Using Bidirectional Mendelian Randomization. Arthritis & Rheumatology. 2021. PMID 33982892. DOI 10.1002/art.41779.

    Mendelian randomization · Genetically higher fasting insulin raised serum urate by 0.37 mg/dL per log unit (0.69 adjusted for BMI); genetically higher urate did not change fasting insulin; hyperinsulinemia leads to hyperuricemia, not the reverse.

  5. 5.

    FitzGerald JD, Dalbeth N, Mikuls T, et al.. 2020 American College of Rheumatology Guideline for the Management of Gout. Arthritis Care & Research. 2020. PMID 32391934. DOI 10.1002/acr.24180.

    Guideline · Treat-to-target serum urate below 6 mg/dL in gout; asymptomatic hyperuricemia defined as 6.8 mg/dL or more without flare or tophus, with a conditional recommendation against pharmacologic urate lowering (24 treated for 3 years to prevent one flare); lifestyle and medication recommendations with their effect sizes.

  6. 6.

    Dalbeth N, Phipps-Green A, Frampton C, Neogi T, Taylor WJ, Merriman TR. Relationship between serum urate concentration and clinically evident incident gout: an individual participant data analysis. Annals of the Rheumatic Diseases. 2018. PMID 29463518. DOI 10.1136/annrheumdis-2017-212288.

    Prospective cohort · 18,889 gout-free participants in four US cohorts: 15-year cumulative gout incidence 1.1 percent below 6 mg/dL to 49 percent at 10 or more; adjusted hazard ratios 2.7, 6.6, 15, 30 and 64 for 6.0 to 6.9, 7.0 to 7.9, 8.0 to 8.9, 9.0 to 9.9 and 10 or more.

  7. 7.

    Campion EW, Glynn RJ, DeLabry LO. Asymptomatic hyperuricemia. Risks and consequences in the Normative Aging Study. American Journal of Medicine. 1987. PMID 3826098. DOI 10.1016/0002-9343(87)90441-4.

    Prospective cohort · 2,046 healthy men followed 14.9 years: annual gout incidence 4.9 percent at urate 9 mg/dL or more, 0.5 percent at 7.0 to 8.9, 0.1 percent below 7.0; 22 percent cumulative at five years above 9; no renal deterioration attributable to hyperuricemia.

  8. 8.

    Kim SY, Guevara JP, Kim KM, Choi HK, Heitjan DF, Albert DA. Hyperuricemia and coronary heart disease: a systematic review and meta-analysis. Arthritis Care & Research. 2010. PMID 20191515. DOI 10.1002/acr.20065.

    Systematic review and meta-analysis · 26 prospective studies, 402,997 adults: adjusted risk ratio 1.09 for coronary heart disease incidence and 1.16 for coronary mortality; 1.12 per mg/dL; mortality excess in women (1.67) but not men.

  9. 9.

    Zhao G, Huang L, Song M, Song Y. Baseline serum uric acid level as a predictor of cardiovascular disease related mortality and all-cause mortality: a meta-analysis of prospective studies. Atherosclerosis. 2013. PMID 24125412. DOI 10.1016/j.atherosclerosis.2013.08.023.

    Systematic review and meta-analysis · 11 prospective studies, 172,123 participants: highest urate category carried relative risk 1.24 for all-cause and 1.37 for cardiovascular mortality; all-cause excess in men (1.23) not women (1.05); very low urate inconclusive.

  10. 10.

    Li X, Meng X, Timofeeva M, et al.. Serum uric acid levels and multiple health outcomes: umbrella review of evidence from observational studies, randomised controlled trials, and Mendelian randomisation studies. BMJ. 2017. PMID 28592419. DOI 10.1136/bmj.j2376.

    Systematic review and meta-analysis · 136 outcomes: no observational association convincing, five highly suggestive; 55 percent of observational meta-analyses showed small-study effects; convincing evidence of a clear role of urate only for gout (Mendelian randomization) and nephrolithiasis recurrence (trials of urate lowering).

  11. 11.

    Keenan T, Zhao W, Rasheed A, et al.. Causal Assessment of Serum Urate Levels in Cardiometabolic Diseases Through a Mendelian Randomization Study. Journal of the American College of Cardiology. 2016. PMID 26821629. DOI 10.1016/j.jacc.2015.10.086.

    Mendelian randomization · 14 urate-specific variants: a 1 SD genetic increase in urate was not associated with type 2 diabetes (26,488 cases), coronary heart disease (54,501), ischemic stroke (14,779) or heart failure (4,526), but raised gout odds 5.84-fold.

  12. 12.

    Jordan DM, Choi HK, Verbanck M, et al.. No causal effects of serum urate levels on the risk of chronic kidney disease: A Mendelian randomization study. PLoS Medicine. 2019. PMID 30645594. DOI 10.1371/journal.pmed.1002725.

    Mendelian randomization · No causal effect of urate on eGFR or CKD across all analyses, with more than 99 percent power; observational association -1.99 mL/min eGFR and CKD odds 1.48 per mg/dL; gout odds 3.41 to 6.04 per mg/dL as positive control.

  13. 13.

    Kimura K, Hosoya T, Uchida S, et al.; FEATHER Study Investigators. Febuxostat Therapy for Patients With Stage 3 CKD and Asymptomatic Hyperuricemia: A Randomized Trial. American Journal of Kidney Diseases. 2018. PMID 30177485. DOI 10.1053/j.ajkd.2018.06.028.

    Randomized trial · 467 patients with stage 3 CKD and asymptomatic hyperuricemia, 108 weeks: eGFR slope 0.23 versus -0.47 mL/min/1.73 m2 per year (difference 0.70, CI -0.21 to 1.62, P = 0.1); gouty arthritis 0.91 versus 5.86 percent.

  14. 14.

    Badve SV, Pascoe EM, Tiku A, et al.; CKD-FIX Study Investigators. Effects of Allopurinol on the Progression of Chronic Kidney Disease. New England Journal of Medicine. 2020. PMID 32579811. DOI 10.1056/NEJMoa1915833.

    Randomized trial · 369 adults with stage 3 or 4 CKD at risk of progression, mean urate 8.2 mg/dL, 104 weeks: eGFR change -3.33 versus -3.23 mL/min per year (difference -0.10, P = 0.85).

  15. 15.

    Doria A, Galecki AT, Spino C, et al.; PERL Study Group. Serum Urate Lowering with Allopurinol and Kidney Function in Type 1 Diabetes. New England Journal of Medicine. 2020. PMID 32579810. DOI 10.1056/NEJMoa1916624.

    Randomized trial · 530 adults with type 1 diabetes and early kidney disease, 3 years: urate 6.1 to 3.9 mg/dL on treatment versus 6.1 on placebo; measured GFR difference 0.001 mL/min; albumin excretion 40 percent higher with treatment.

  16. 16.

    Narang RK, Gamble GG, Topless R, et al.. Assessing the Relationship Between Serum Urate and Urolithiasis Using Mendelian Randomization: An Analysis of the UK Biobank. American Journal of Kidney Diseases. 2021. PMID 33400963. DOI 10.1053/j.ajkd.2020.11.018.

    Mendelian randomization · 359,827 participants, 6,398 (1.8 percent) with urolithiasis: unadjusted odds 1.47, adjusted 1.03; two-stage MR odds 0.93; no causal effect of serum urate on stones.

  17. 17.

    Cho SK, Chang Y, Kim I, Ryu S. U-Shaped Association Between Serum Uric Acid Level and Risk of Mortality: A Cohort Study. Arthritis & Rheumatology. 2018. PMID 29694719. DOI 10.1002/art.40472.

    Prospective cohort · 375,163 South Korean adults, 2,020 deaths: all-cause mortality hazard 1.58 (men below 3.5 mg/dL) and 1.80 (women below 2.5); 2.39 (men 9.5 or more) and 3.77 (women 8.5 or more).

  18. 18.

    Choi HK, Curhan G. Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. BMJ. 2008. PMID 18244959. DOI 10.1136/bmj.39449.819271.BE.

    Prospective cohort · 46,393 men, 12 years, 755 cases: two or more sugar-sweetened soft drinks a day relative risk 1.85; top fifth of fructose 2.02; diet soft drinks no association.

  19. 19.

    Choi HK, Willett W, Curhan G. Fructose-rich beverages and risk of gout in women. JAMA. 2010. PMID 21068145. DOI 10.1001/jama.2010.1638.

    Prospective cohort · 78,906 women, 22 years, 778 cases: two or more sugar-sweetened sodas a day relative risk 2.39, orange juice 2.42; absolute excess 68 and 47 cases per 100,000 person-years; diet soft drinks no association.

  20. 20.

    Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G. Alcohol intake and risk of incident gout in men: a prospective study. Lancet. 2004. PMID 15094272. DOI 10.1016/S0140-6736(04)16000-5.

    Prospective cohort · 47,150 men, 12 years, 730 cases: relative risk 1.49 at 15 to 29.9 g alcohol a day and 2.53 at 50 or more; per daily beer 1.49, per shot of spirits 1.15, per glass of wine 1.04.

  21. 21.

    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. PMID 15014182. DOI 10.1056/NEJMoa035700.

    Prospective cohort · 47,150 men, 12 years: highest fifth of meat relative risk 1.41, seafood 1.51, dairy 0.56; purine-rich vegetables and total protein not associated.

  22. 22.

    Nielsen SM, Bartels EM, Henriksen M, et al.. Weight loss for overweight and obese individuals with gout: a systematic review of longitudinal studies. Annals of the Rheumatic Diseases. 2017. PMID 28866649. DOI 10.1136/annrheumdis-2017-211472.

    Systematic review and meta-analysis · 10 studies (one randomized), weight loss 3 to 34 kg: urate change -168 to +30 µmol/L; 0 to 60 percent reached below 360 µmol/L; six of eight studies fewer attacks; transient rise after bariatric surgery; low-quality evidence.

  23. 23.

    McAdams DeMarco MA, Maynard JW, Baer AN, et al.. Diuretic use, increased serum urate levels, and risk of incident gout in a population-based study of adults with hypertension: the Atherosclerosis Risk in Communities cohort study. Arthritis & Rheumatism. 2012. PMID 22031222. DOI 10.1002/art.33315.

    Prospective cohort · 5,789 adults with hypertension: starting a diuretic raised urate 0.72 mg/dL more than not starting; gout hazard 1.48 (thiazide 1.44, loop 2.31), null after adjusting for urate; other antihypertensives 0.64.

  24. 24.

    Gohari S, Ghobadi S, Jafari A, Ahangar H, Gohari S, Mahjani M. The effect of dietary approaches to stop hypertension and ketogenic diets intervention on serum uric acid concentration: a systematic review and meta-analysis of randomized controlled trials. Scientific Reports. 2023. PMID 37380733. DOI 10.1038/s41598-023-37672-2.

    Systematic review and meta-analysis · Four DASH trials (590 participants): urate -0.25 mg/dL, no heterogeneity; six ketogenic trials (267): +0.26 mg/dL, CI -0.47 to 0.98, heterogeneity 95 percent.

  25. 25.

    Green HJ, Fraser IG. Differential effects of exercise intensity on serum uric acid concentration. Medicine and Science in Sports and Exercise. 1988. PMID 3343917. DOI 10.1249/00005768-198802000-00008.

    Cross-sectional study · Repeated 1-minute bouts at 120 percent of VO2max raised plasma urate 40 percent, with next-day resting values 476 versus 352 µmol/L; 2 hours at 65 percent did not raise it; intensity, not total work, drives the rise.

  26. 26.

    Ricós C, Alvarez V, Cava F, et al.. Desirable Biological Variation Database specifications (2014 update of the Ricós database). Westgard QC. 2014.

    Laboratory method study · Serum urate: within-subject biological variation 8.6 percent, between-subject 17.5 percent (16 papers).

  27. 27.

    Aarsand AK, Díaz-Garzón J, Fernandez-Calle P, et al.; EFLM Working Group on Biological Variation. The EuBIVAS: Within- and Between-Subject Biological Variation Data for Electrolytes, Lipids, Urea, Uric Acid, Total Protein, Total Bilirubin, Direct Bilirubin, and Glucose. Clinical Chemistry. 2018. PMID 29941472. DOI 10.1373/clinchem.2018.288415.

    Laboratory method study · 91 healthy adults sampled weekly for 10 weeks: within-subject variation for uric acid differed significantly between men and women.

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