Uric Acid Test: Ranges, Results & What They Mean
Your physician orders routine blood work, and tucked away in the results is a line for uric acid. Most patients skip right past it, figuring it’s only a concern if they have gout.
Big mistake.
Getting your uric acid tested gives insight into much more than joint issues. It’s now connected to cardiovascular disease, kidney damage, diabetes and even mental decline, often well before you realize there’s a problem.
What You Should Know
- Uric acid tests measure a waste product from purine breakdown that affects multiple body systems
- Optimal levels (below 5.5 mg/dL) differ significantly from standard “normal” laboratory ranges (up to 7-8 mg/dL)
- Blood tests provide the most common measurement, while 24-hour urine collection reveals production versus excretion patterns
- About 14.6% of US adults have elevated uric acid (hyperuricemia), though 85-90% never develop gout symptoms
What is a Uric Acid Test?
A uric acid test measures the concentration of uric acid in your blood or urine. Your body creates this waste product when it breaks down purines, chemical compounds found in certain foods (red meat, organ meats, seafood) and naturally present in your cells.
The test uses one of two methods. The enzymatic approach (now the gold standard) employs the enzyme uricase to oxidize uric acid, creating a chemical reaction that allows precise measurement. The older colorimetric method measures color change but can overestimate levels by about 1 mg/dL due to interference from other substances like vitamin C.
Your kidneys normally filter uric acid from blood and eliminate it through urine. When your body produces too much or your kidneys remove too little, levels climb in your bloodstream.
Why Uric Acid Levels Matter for Your Health
Most physicians learned about uric acid in the context of two conditions: gout and kidney stones. That narrow focus misses the bigger picture emerging from recent research.
Dr. Richard Johnson is a Professor of Medicine at the University of Colorado Denver, who has authored over 400 articles exploring the role of fructose metabolism in causing obesity, diabetes and kidney disease through the production of uric acid. He found that when we ingest fructose, it produces uric acid within the cells of our body. The resulting uric acid then triggers metabolic pathways that increase fat storage and insulin resistance.
“Our work focuses on how diet (and in particular fructose) may have a role in the epidemics of obesity, diabetes, hypertension and kidney disease, and how those sugars may cause their metabolic effects by raising uric acid levels,” Johnson explained.
This mechanism is an evolutionary adaptation. Uric acid was once a metabolic switch that enabled our ancient ancestors to store fat and survive when food was scarce. Today we never have to go without food (particularly fructose that is added to our processed foods) and the adaptation becomes a detriment.

The Gout Connection
Gout remains the most recognized consequence of a high level of uric acid. The condition occurs when uric acid crystals deposit in joints and soft tissues, triggering sudden, severe pain and inflammation.
The relationship between high uric acid and gout is more complex than most realize. Approximately 85-90% of people with hyperuricemia never develop gout1. Conversely, up to 39% of gout patients show normal uric acid levels during acute attacks because levels temporarily drop as uric acid crystals precipitate from blood into joints2.
Global gout prevalence ranges from 1-4%, but the United States shows the highest burden worldwide with 5.1% of adults affected (about 12.1 million people as of 2017-2018)3. That number jumped from 3.9% just two years earlier, representing nearly 3 million more cases.
Between 2001 and 2021, disability rates from gout in the US nearly doubled. Geographic patterns show clustering in Hawaii, South Carolina, Alabama, and Louisiana, with Hawaii’s rates exceeding double the national average.
Cardiovascular and Metabolic Risk
The cardiovascular connection carries serious implications. Research cited by Dr. David Perlmutter, board-certified neurologist and author of Drop Acid, reveals that for every 1 mg/dL increase in uric acid above 7, all-cause mortality rises 8-13%. Death from cardiovascular disease increases 38%, and stroke risk climbs 35%.
A 2018 study examining 90,000 adults found that uric acid levels above 5.5 mg/dL correlate with increased cardiovascular and metabolic risk, well below the point where gout typically develops4. Dr. Mimi Guarneri, cardiologist and founder of the Academy of Integrative Health and Medicine, routinely checks patients’ uric acid “because of the links with cardiovascular disease.”
The metabolic syndrome connections extend across multiple conditions. A 2023 meta-analysis found that among people with hyperuricemia, 65% had non-alcoholic fatty liver disease compared to much lower rates in those with normal levels. The pooled data showed 1.88 times higher risk of developing fatty liver with elevated uric acid5.
Recent research published in Signal Transduction and Targeted Therapy notes that 43.3 million Americans have hyperuricemia, representing a sharp rise since 19606. The paper links elevated levels to “a spectrum of commodities such as gout, cardiovascular diseases, renal disorders, metabolic syndrome, and diabetes.”
Kidney Disease Links
Multiple large-scale studies demonstrate that elevated uric acid predicts chronic kidney disease development independent of traditional risk factors. A 2008 study following 21,475 healthy volunteers for seven years found that slightly elevated levels (7.0-8.9 mg/dL) nearly doubled the risk for new kidney disease7.
The mechanism differs from gout’s crystal-dependent process. As Dr. Johnson and colleagues discovered, “When laboratory animals with CKD were made hyperuricemic, the renal disease progressed rapidly despite an absence of crystals in the kidney.” Soluble uric acid, not just crystals, drives kidney damage through inflammatory, oxidative, and vascular pathways8.
A 2014 meta-analysis of 15 cohort studies confirmed a positive association between serum uric acid and chronic kidney disease risk in middle-aged patients, independent of established metabolic risk factors9.
Types of Uric Acid Tests
Three testing approaches offer different insights into uric acid metabolism.
Blood (Serum) Test
The uric acid blood test is the most common diagnostic tool, measuring uric acid concentration in blood serum. A healthcare provider draws blood from a vein (typically in your inner elbow or back of hand) and sends it to a laboratory for analysis.
The procedure takes just a few minutes and causes minimal discomfort. You can usually eat and drink normally before the test, though certain medications may affect results (discussed below).
Results typically return within one to three days, depending on the laboratory. The uric acid blood test provides a snapshot of your current levels, making it useful for monitoring treatment and tracking changes over time.
24-Hour Urine Collection
The uric acid urine test offers a comprehensive assessment, measuring total uric acid your body excretes over a full day. This test helps determine whether high blood levels result from overproduction or inadequate kidney excretion, information that guides treatment decisions.
You collect all urineproduced during exactly 24 hours in a special container with preservative, storing samples refrigerated. The lab then measures total uric acid in the combined sample.
This uric acid urine test requires more effort but provides valuable metabolic information blood tests can’t reveal. Avoid alcohol during collection (it reduces kidney uric acid excretion) and maintain normal hydration.
At-Home Testing Options
Emerging point-of-care devices enable home monitoring similar to glucose testing for diabetes. These finger-prick devices provide results within minutes.
Dr. Perlmutter recommends the UASure at-home test kit for regular monitoring, suggesting testing each morning before eating with a target reading of 5.5 mg/dL or lower. This approach allows you to track how dietary changes affect your levels over time.
Home testing kits like Jinfiniti’s AgingSOS offer convenience but shouldn’t replace professional medical evaluation when needed. Use it as a monitoring tool between regular checkups.
Understanding Your Test Results
Reference ranges on lab reports can mislead if you don’t understand what “normal” actually means.
Standard Reference Ranges
Laboratory reference ranges typically show:
| Gender | Standard Range (mg/dL) | Alternative Range (µmol/L) |
|---|---|---|
| Males | 2.5-7.0 or 4.0-8.6 | 208-400 |
| Females | 1.5-6.0 or 3.0-7.1 | 155-400 |
Mayo Clinic Laboratory sets reference values for males ages 13 and above at 2.7-6.1 mg/dL. These ranges vary slightly among laboratories.
More importantly, they were derived primarily based on gout risk, the point where uric acid begins crystallizing in joints and blood vessels.
The Optimal Level Debate
A significant gap exists between laboratory “normal” ranges and optimal health targets.
Dr. Perlmutter strongly advocates for more stringent targets. “The optimal level is below 5.5, so it’s significantly lower [than 7 mg/dL],” he states. “The cardiometabolic issues begin at 5.5.”
The traditional ranges relate to gout, the point above 7 mg/dL where uric acid precipitates into crystals. But metabolic dysfunction starts well before crystals form.
At Jinfiniti Precision Medicine, founder Dr. Jin-Xiong She explains the importance of this distinction: “We include uric acid in our AgingSOS panels because it serves as an early warning system for metabolic dysfunction. When we see levels creeping above 5.5 mg/dL, even if still within the laboratory reference range, we know cellular metabolism is already being affected. This allows us to intervene before diseases like diabetes or cardiovascular problems develop.”
Dr. Giovanni Desideri and colleagues, writing in European Heart Journal, advocate that “a threshold value < 6.0 mg/dL (< 360 µmol/L) seems to better identify true ‘healthy subjects’ and should reasonably be considered for all subjects.”4
This represents a paradigm shift toward preventive medicine focused on optimal rather than merely “normal” values.
What High Levels Mean
Hyperuricemia is clinically defined as levels exceeding 6.8 mg/dL, the saturation point where urate becomes supersaturated at normal body temperature. Mayo Clinic defines it as greater than 6.0 mg/dL in women and 7.0 mg/dL in men.
A high uric acid level can result from:
- Overproduction: Diet high in purines, rapid cell turnover (cancer, chemotherapy), genetic factors, or fructose consumption
- Underexcretion: Impaired kidney function, dehydration, certain medications (diuretics, low-dose aspirin), or metabolic conditions
About 14.6% of US adults (approximately 32.5 million people) have hyperuricemia, though most remain asymptomatic.
What Low Levels Mean
While high levels receive most attention, a low uric acid level can also indicate problems. Ranges below 2.0 mg/dL may suggest:
- Wilson’s disease (genetic copper metabolism disorder)
- Fanconi syndrome (kidney tubule dysfunction)
- Certain medications
- Low-purine diet combined with high fluid intake
Recent research proposes the concept of “dysuricemia,” recognizing that both excessively high and low levels represent pathological states. At physiological concentrations around 5 mg/dL, uric acid demonstrates antioxidant effects by scavenging free radicals. Above 5.5-6.0 mg/dL, it promotes inflammation and cellular damage.
A low uric acid level may seem harmless, but extremely low values can indicate underlying health conditions requiring medical attention.
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When Should You Get a Uric Acid Test?
Healthcare providers order uric acid tests under specific circumstances:
- You have unexplained joint pain, particularly sudden severe pain with redness and swelling in your big toe. Recurrent attacks of joint inflammation warrant testing even if previous tests were normal (levels can drop during acute flares).
- Your doctor monitors you during chemotherapy or radiation. Rapid cell turnover releases large amounts of purines, sometimes causing dangerous spikes requiring intervention.
- You experience recurrent kidney stones. About 10-15% of kidney stones contain uric acid, and testing helps determine if elevated levels contribute to stone formation.
- You’re assessing cardiovascular or metabolic risk. Given emerging research on uric acid’s role in heart disease, diabetes, and metabolic syndrome, progressive practitioners include it in comprehensive health assessments.
- You’re investigating symptoms like blood in urine, frequent urination, sharp back or side pain, or unexplained fatigue that might indicate kidney dysfunction.
- You have conditions associated with altered uric acid levels: chronic kidney disease, diabetes, hypertension, or metabolic syndrome.
Testing makes particular sense if you’re focused on longevity and healthy aging since uric acid provides early warning of metabolic dysfunction before disease develops.
How to Prepare for the Test
Blood tests generally require no special preparation. You can eat and drink normally before testing.
Certain medications affect results and should be reported to your healthcare provider:
- Aspirin and other salicylates
- Ibuprofen and NSAIDs
- Diuretics (water pills)
- Niacin supplements
- Gout medications (allopurinol, probenecid)
- Some blood pressure medications
Don’t stop prescribed medications without consulting your doctor. Simply inform the provider so they can interpret results appropriately.
For 24-hour urine collection, avoid alcohol during the collection period since it reduces kidney excretion of uric acid. Maintain your normal diet and hydration unless instructed otherwise.
The blood draw itself follows standard venipuncture procedure. After sterilizing the site, the provider wraps an elastic band around your arm to fill veins, inserts a needle to draw blood into vials, then removes the band and needle and applies pressure with a bandage. Minor bruising may occur but typically resolves quickly.
What Affects Uric Acid Levels?
Multiple factors influence your test results beyond underlying health conditions.
Diet and Fructose
Fructose stands out as the primary dietary driver of elevated uric acid. Unlike glucose, fructose metabolism uniquely generates uric acid inside cells through a process that depletes cellular energy (ATP).
Dr. Perlmutter emphasizes this connection: “Uric acid is not just the cause of gout; it is intricately linked with the processes involved in weight gain, fat accumulation.”
Major dietary sources that raise uric acid:
- High-fructose corn syrup in sodas and processed foods (a single can of regular soda contains about 23 grams of fructose)
- Table sugar/sucrose (50% fructose content)
- Fruit juice in large amounts
- Red meat and organ meats (liver, kidney)
- Certain seafood (anchovies, sardines, mussels, scallops)
- Some vegetables (asparagus, spinach)
- Beer and other alcoholic beverages
Alcohol is particularly problematic because it both increases uric acid production and decreases kidney excretion.
The impact of diet on NAD+ levels and cellular health connects to uric acid metabolism since both involve how your body processes nutrients for energy.
Medications and Supplements
Many common medications affect uric acid levels:
Medications that increase levels:
- Diuretics (especially thiazides)
- Low-dose aspirin
- Niacin
- Cyclosporine
- Levodopa
Medications that decrease levels:
- Allopurinol
- Febuxostat
- Probenecid
- Losartan
- High-dose vitamin C
Always inform your healthcare provider about all medications and supplements before testing. The effect doesn’t necessarily mean you should stop the medication, just that results should be interpreted in that context.
Medical Conditions
Various health conditions alter uric acid metabolism:
Conditions that increase levels:
- Chronic kidney disease
- Diabetes
- Metabolic syndrome
- Hypertension
- Psoriasis
- Hypothyroidism
- Certain cancers
- Obesity
Conditions that decrease levels:
- Liver disease
- Wilson’s disease
- Fanconi syndrome
- SIADH (syndrome of inappropriate antidiuretic hormone)
Dehydration temporarily concentrates uric acid in blood. Strenuous exercise can cause transient elevations through muscle breakdown and dehydration.
Understanding these factors helps distinguish between concerning chronic elevations and temporary fluctuations. This connects to broader patterns of oxidative stress and metabolic dysfunction that affect multiple body systems.
The Role of Uric Acid Testing in Gout Management
For those with diagnosed gout, uric acid testing guides treatment decisions.
The 2020 American College of Rheumatology guidelines establish a treat-to-target approach with specific recommendations10:
Treatment targets:
- Standard goal: Below 6 mg/dL for most gout patients
- Severe disease goal: Below 5 mg/dL for patients with tophi (visible uric acid deposits)
- Serial monitoring: Regular testing to guide medication dose adjustments
The test isn’t definitive for diagnosing gout, though. Only analyzing joint fluid for monosodium urate crystals conclusively confirms the condition. Synovial fluid analysis using polarized light microscopy shows the characteristic needle-shaped, negatively birefringent crystals.
Key testing considerations for gout:
- Up to 39% of gout patients show normal uric acid during acute attacks
- Levels drop temporarily as crystals precipitate from blood into joints
- Repeat testing or joint fluid analysis may be needed if clinical suspicion remains high
- Regular monitoring after starting treatment ensures medication effectiveness
Despite clear guidelines, evidence shows delivery of gout care remains suboptimal. A 2015 study found that among Americans with gout receiving urate-lowering therapy, only a minority achieved the target level below 6 mg/dL11. Inadequate dose titration and poor adherence contribute to this treatment gap.
Current Research and Uric Acid’s Dual Nature
Recent research reveals uric acid’s paradoxical properties. At concentrations around 5 mg/dL, it demonstrates protective antioxidant effects by scavenging free radicals. Above 5.5-6.0 mg/dL, it promotes cellular senescence, inflammation, and oxidative damage.
Key findings from genetic studies:
Sophisticated genetic studies using Mendelian randomization (examining genetic variants affecting uric acid levels) have yielded mixed results on causality. Several studies found no direct causal relationship between elevated uric acid and risks of diabetes, coronary heart disease, or stroke.
“The only phenotypes that were causally associated with [hyperuricemia] were gout and kidney disease,” according to a 2024 review. Yet clinical and epidemiological studies consistently link hyperuricemia with cardiovascular disease, fatty liver, hypertension, insulin resistance, and obesity.
This suggests uric acid may be a marker of underlying metabolic dysfunction even if not always the direct cause.
Promising intervention trials:
Clinical trials examining whether lowering uric acid improves outcomes show promise in specific populations. A 2022 meta-analysis of febuxostat (a urate-lowering medication) in chronic kidney disease patients demonstrated significant benefits12:
- Serum uric acid decreased by 146 µmol/L
- Kidney function (estimated glomerular filtration rate) improved by 3.21 mL/min
- Serum creatinine decreased by 15.27 µmol/L
- Serum urea nitrogen fell by 2.37 mmol/L
This emerging understanding parallels research on cellular senescence and aging, where multiple interconnected processes contribute to metabolic dysfunction rather than single causes.
Interpreting Results: Beyond the Numbers
Your test results tell a story beyond the number on the report.
When treatment may not be needed:
A single elevated reading doesn’t automatically warrant treatment if you have no symptoms or risk factors. The 2020 ACR guidelines conditionally recommend against treating asymptomatic hyperuricemia even with comorbid cardiovascular disease, kidney disease, or hypertension.
Uncertainty remains about whether treating isolated elevation prevents future complications.
When proactive intervention makes sense:
If you’re focused on optimal health and longevity rather than just disease prevention, targeting levels below 5.5 mg/dL makes sense based on current research. This proactive approach aligns with precision medicine principles, addressing dysfunction before disease develops.
What to consider when reviewing your results:
- Serial measurements provide more value than single readings
- Trending upward over time signals worsening metabolic function
- Your full clinical picture matters: family history, cardiovascular risk factors, kidney function, diet quality
- Other biomarkers of aging provide context
Uric acid represents one piece of the metabolic health puzzle. The comprehensive assessment matters.
That’s why Jinfiniti includes uric acid alongside 27 other biomarkers in the AgingSOS Advanced Panel, providing the full metabolic context needed for truly personalized health optimization.
Test Uric Acid With Jinfiniti’s AgingSOS Panel
Jinfiniti’s AgingSOS Advanced Panel measures uric acid alongside rare biomarkers not routinely tested elsewhere, including intracellular NAD+ and klotho (the longevity protein).
What the comprehensive panel includes:
- 28 total biomarkers covering multiple health systems
- Inflammation status markers
- Oxidative stress measurements
- Cellular senescence indicators
- Metabolic health metrics
- Cardiovascular risk factors
The panel detects issues years before symptoms appear, allowing early intervention. Each test includes a free consultation to review results and develop a personalized optimization plan.
Convenient testing options:
- Mobile phlebotomy available for at-home blood collection
- CLIA-certified laboratory processing
- Results typically within 1-2 weeks
- Personalized interpretation and recommendations
The TAO approach in action:
The testing philosophy follows Jinfiniti’s TAO approach: Test to establish baseline, Act with targeted interventions based on results, and Optimize through continuous monitoring and adjustment.
Rather than treating individual biomarkers in isolation, the comprehensive panel reveals how systems interact. Your uric acid level makes more sense when viewed alongside inflammation markers, kidney function, metabolic indicators, and cellular health measurements.
Referenced Sources
- Zhang, W.-Z. Why Does Hyperuricemia Not Necessarily Induce Gout?Biomolecules vol. 11 280 https://doi.org/10.3390/biom11020280 (2021).
- Leiszler, M., Poddar, S. & Fletcher, A. Clinical inquiry. Are serum uric acid levels always elevated in acute gout? Journal of Family Practice 60 10, 618–20 (2011).
- Singh, G., Lingala, B. & Mithal, A. Gout and Hyperuricaemia in the USA: Prevalence and Trends. Rheumatology vol. 58 2177–2180 https://doi.org/10.1093/rheumatology/kez196 (2019).
- Desideri, G. et al. Is it time to revise the normal range of serum uric acid levels? European Review for Medical and Pharmacological Sciences 18 9, 1295–306 (2014).
- Sun, Q. et al. Association Between Serum Uric Acid and Non-Alcoholic Fatty Liver Disease: An Updated Systematic Review and Meta-Analysis. Clinical Epidemiology vol. Volume 15 683–693 https://doi.org/10.2147/clep.s403314 (2023).
- Du, L. et al. Hyperuricemia and Its Related Diseases: Mechanisms and Advances in Therapy. Signal Transduction and Targeted Therapy vol. 9 https://doi.org/10.1038/s41392-024-01916-y (2024).
- Obermayr, R. P. et al.Elevated Uric Acid Increases the Risk for Kidney Disease. Journal of the American Society of Nephrology vol. 19 2407–2413 https://doi.org/10.1681/asn.2008010080 (2008).
- Johnson, R. J. et al. Uric Acid and Chronic Kidney Disease: Which Is Chasing Which?Nephrology Dialysis Transplantation vol. 28 2221–2228 https://doi.org/10.1093/ndt/gft029 (2013).
- Zhu, P., Liu, Y., Han, L., Xu, G. & Ran, J. Serum Uric Acid Is Associated with Incident Chronic Kidney Disease in Middle-Aged Populations: A Meta-Analysis of 15 Cohort Studies. PLoS ONE vol. 9 e100801 https://doi.org/10.1371/journal.pone.0100801 (2014).
- FitzGerald, J. D. et al. 2020 American College of Rheumatology Guideline for the Management of Gout. Arthritis & Rheumatology vol. 72 879–895 https://doi.org/10.1002/art.41247 (2020).
- Juraschek, S. P., Kovell, L. C., Miller, E. R. & Gelber, A. C. Gout, Urate‐Lowering Therapy, and Uric Acid Levels Among Adults in the United States. Arthritis Care & Research vol. 67 588–592 https://doi.org/10.1002/acr.22469 (2015).
- Zheng, Y. & Sun, J. Febuxostat Improves Uric Acid Levels and Renal Function in Patients with Chronic Kidney Disease and Hyperuricemia: A Meta-Analysis. Applied Bionics and Biomechanics vol. 2022 1–7 https://doi.org/10.1155/2022/9704862 (2022).
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