Uric Acid
Uric acid is the final breakdown product of purines (from cell turnover and diet). Kidneys excrete ~70%. When levels exceed solubility, uric acid crystallizes — causing gout (joint crystals) and kidney stones. Most hyperuricemia is from under-excretion (kidneys, diuretics) rather than overproduction. High uric acid is strongly associated with metabolic syndrome, hypertension, cardiovascular disease, and kidney disease. Dietary culprits: red meat, organ meats, shellfish, beer, fructose.
Uric acid is the final breakdown product of purines — compounds found in your body’s cells and in certain foods. Normally, uric acid dissolves in blood, passes through the kidneys, and leaves the body in urine. When uric acid levels become too high, it can crystallize and deposit in joints (causing gout), form kidney stones, and contribute to kidney disease.
Why does this matter? Elevated uric acid (hyperuricemia) is incredibly common and increasingly recognized as more than just a gout risk. It’s strongly associated with metabolic syndrome, hypertension, cardiovascular disease, and chronic kidney disease. Whether uric acid directly causes these conditions or is simply a marker is still debated, but its presence signals increased health risk.
Uric acid testing helps diagnose gout, monitor treatment effectiveness, assess kidney stone risk, and evaluate overall metabolic health. It’s a valuable piece of the metabolic puzzle.
Key Benefits of Testing
Uric acid testing identifies people at risk for gout — a painful inflammatory arthritis that can be prevented with proper management. For those who’ve had gout attacks, monitoring guides treatment to reduce levels and prevent future flares.
Beyond gout, this test provides metabolic health information. Elevated uric acid often accompanies obesity, insulin resistance, and hypertension — identifying it prompts evaluation for these related conditions and their management.
What Does This Test Measure?
Uric acid measures the concentration of this compound in your blood serum. Your lab provides results alongside their reference range, which typically differs between men and women.
Where Uric Acid Comes From
Uric acid is produced from purine breakdown:
Endogenous production (~70%): Your body constantly produces and breaks down purines during normal cell turnover. Dying cells release purines that become uric acid.
Dietary intake (~30%): Foods high in purines contribute to uric acid production. Red meat, organ meats, shellfish, and certain fish are high in purines. Beer and spirits also raise uric acid.
How Uric Acid Leaves the Body
Kidneys (~70%): The kidneys filter uric acid from blood and excrete it in urine. Most people with high uric acid are “under-excreters” — their kidneys don’t eliminate enough.
Gut (~30%): Some uric acid is eliminated through the intestines.
The Solubility Problem
Uric acid has limited solubility in blood. When levels exceed the saturation point, uric acid can crystallize — especially in cooler areas like joints in the feet (hence gout often affects the big toe). These needle-shaped crystals trigger intense inflammation.
Why This Test Matters
Diagnoses and Monitors Gout
Gout is caused by uric acid crystal deposition in joints. While a gout attack can occur even with “normal” uric acid levels (crystals formed earlier), persistently elevated levels increase attack risk. Treatment aims to lower uric acid below the crystallization threshold to dissolve existing deposits and prevent new ones.
Assesses Kidney Stone Risk
Uric acid stones account for about 10% of kidney stones. High blood uric acid increases risk, particularly when urine is acidic. Monitoring helps guide prevention strategies.
Reflects Kidney Function
Since kidneys excrete most uric acid, rising levels can indicate declining kidney function. Uric acid itself may also contribute to kidney damage — a bidirectional relationship.
Signals Metabolic Risk
Elevated uric acid is strongly associated with:
- Metabolic syndrome
- Insulin resistance and type 2 diabetes
- Hypertension
- Cardiovascular disease
- Non-alcoholic fatty liver disease
Whether uric acid causes these conditions or results from them is unclear, but its presence identifies people who need comprehensive metabolic evaluation.
Monitors Tumor Lysis Risk
When cancer cells are destroyed rapidly (by chemotherapy), they release massive amounts of purines, spiking uric acid dangerously high. Monitoring prevents acute uric acid nephropathy.
What Can Affect Your Uric Acid?
Causes of High Uric Acid (Hyperuricemia)
Decreased excretion (most common):
- Chronic kidney disease — reduced filtration and excretion
- Medications — diuretics (thiazides, loop), low-dose aspirin, cyclosporine, tacrolimus
- Metabolic syndrome and insulin resistance — insulin reduces kidney uric acid excretion
- Hypothyroidism
- Lead exposure
- Alcohol — especially beer (contains purines AND reduces excretion)
- Dehydration — concentrates uric acid
Increased production:
- High-purine diet — red meat, organ meats, shellfish, sardines, anchovies
- Fructose and sugar-sweetened beverages — increase purine synthesis
- Rapid cell turnover — psoriasis, hemolytic anemia, myeloproliferative disorders
- Tumor lysis syndrome — cancer treatment releasing purines
- Genetic disorders of purine metabolism (rare)
Associated conditions:
- Obesity
- Hypertension
- Diabetes
- Heart failure
- Preeclampsia
Causes of Low Uric Acid (Hypouricemia)
Increased excretion:
- Genetic defects in uric acid transporters (rare)
- Fanconi syndrome
- SIADH
- Medications — losartan, high-dose aspirin, probenecid
Decreased production:
- Xanthine oxidase deficiency (very rare)
- Severe liver disease
- Low-purine diet
Testing Considerations
Fasting is often recommended as recent food intake can affect levels. Alcohol should be avoided before testing. Levels may be lower during an acute gout attack (uric acid moves into crystals). Men typically have higher levels than women until menopause.
When Should You Get Tested?
Joint Pain Suggestive of Gout
Sudden, severe joint pain — especially in the big toe, ankle, or knee — with redness and swelling warrants uric acid testing. Classic gout attacks peak within 24 hours.
History of Gout
After gout diagnosis, regular monitoring guides treatment and confirms uric acid is maintained below target.
Kidney Stones
People with kidney stones, especially uric acid stones, benefit from monitoring to guide prevention.
Chronic Kidney Disease
As kidney function declines, uric acid typically rises. Monitoring is part of comprehensive CKD management.
Metabolic Syndrome Components
Those with obesity, hypertension, diabetes, or abnormal lipids may benefit from uric acid assessment as part of metabolic evaluation.
Before Cancer Treatment
Patients at risk for tumor lysis syndrome need baseline uric acid and monitoring during treatment.
Taking Medications Affecting Uric Acid
Diuretics, aspirin, and other medications that raise uric acid warrant periodic monitoring.
Understanding Your Results
Your lab provides reference ranges that differ by sex (men have higher normal values). Interpretation depends on clinical context:
Within reference range: Lower risk for gout and uric acid stones. However, gout can occur even at upper-normal levels if crystals formed previously.
Above reference range (hyperuricemia): Increased risk for gout, kidney stones, and possibly cardiovascular/metabolic disease. Risk increases with degree of elevation. Not everyone with high uric acid develops gout — but risk increases over time.
Below reference range (hypouricemia): Uncommon. May indicate genetic transport defects, kidney tubular disorders, or medications. Very low levels can increase risk for exercise-induced acute kidney injury (rare).
Target Levels for Gout Treatment
For those with gout, the goal is to lower uric acid below the saturation point where crystals dissolve. Treatment targets are typically well below the upper limit of normal to ensure crystals can dissolve and prevent new formation.
Uric Acid During Gout Attacks
Interestingly, uric acid levels can drop during an acute gout attack as uric acid moves from blood into crystal deposits. A “normal” level during an attack doesn’t rule out gout — test again after the attack resolves.
What to Do About Abnormal Results
For Elevated Uric Acid Without Gout (Asymptomatic Hyperuricemia)
Lifestyle modifications:
- Limit high-purine foods (red meat, organ meats, shellfish)
- Reduce or eliminate alcohol, especially beer
- Avoid sugar-sweetened beverages and fructose
- Stay well-hydrated
- Achieve healthy weight — weight loss lowers uric acid
- Consider coffee — associated with lower uric acid
- Consider cherries or cherry juice — may help lower levels
Review medications: If on diuretics, discuss alternatives if possible.
Evaluate for associated conditions: Check blood pressure, glucose, lipids, and kidney function.
Medication generally not recommended: For asymptomatic hyperuricemia without gout, uric acid-lowering medication is typically not indicated — lifestyle modification is first-line.
For Elevated Uric Acid With Gout
Treat acute attacks: NSAIDs, colchicine, or corticosteroids for acute flares.
Start uric acid-lowering therapy: After acute attack resolves, begin treatment to lower uric acid below target. Options include:
- Allopurinol — reduces uric acid production (most common)
- Febuxostat — also reduces production
- Probenecid — increases kidney excretion
Continue lifestyle modifications: Diet and lifestyle changes complement medication.
Monitor and adjust: Regular testing ensures target is achieved and maintained.
For Kidney Stone Prevention
Increase fluid intake: Dilute urine to prevent crystal formation.
Consider urine alkalinization: Uric acid stones form in acidic urine. Potassium citrate can raise urine pH.
Lower uric acid if elevated: With medication if lifestyle changes insufficient.
Related Health Conditions
Gout
Uric Acid Crystal Arthritis: Caused by monosodium urate crystals depositing in joints. Causes sudden, severe pain — classically in the big toe (podagra). Treatable and preventable with uric acid control.
Kidney Stones
Uric Acid Stones: Form when uric acid crystallizes in urine, especially when acidic. Account for about 10% of stones. Preventable with hydration, urine alkalinization, and uric acid control.
Chronic Kidney Disease
Bidirectional Relationship: Kidney disease raises uric acid (reduced excretion), and high uric acid may worsen kidney function. Monitoring and management important in CKD.
Metabolic Syndrome
Cluster of Risk Factors: Hyperuricemia is strongly associated with obesity, insulin resistance, hypertension, and dyslipidemia. Elevated uric acid may be a marker or contributor.
Cardiovascular Disease
Associated Risk: Higher uric acid is associated with increased cardiovascular events. Whether lowering uric acid reduces CV risk is still being studied.
Why Regular Testing Matters
For those with gout, regular uric acid monitoring ensures treatment maintains levels below target, preventing attacks and crystal accumulation. For those with elevated levels without gout, tracking helps assess whether lifestyle changes are working and whether risk is increasing.
Given associations with metabolic and cardiovascular disease, uric acid provides valuable information about overall health risk beyond just gout.
Related Biomarkers Often Tested Together
Creatinine and eGFR — Kidney function affects uric acid excretion.
Glucose and HbA1c — Insulin resistance affects uric acid; diabetes often coexists.
Lipid Panel — Dyslipidemia commonly accompanies hyperuricemia.
hs-CRP — Inflammation marker; elevated during gout attacks.
ALT — Fatty liver often accompanies metabolic syndrome and hyperuricemia.
Note: Information provided in this article is for educational purposes and doesn’t replace personalized medical advice.
Frequently Asked Questions
Uric acid is the final breakdown product of purines — compounds from cell turnover and certain foods. It’s normally excreted by the kidneys. When levels get too high, uric acid can crystallize, causing gout and kidney stones.
Most commonly, the kidneys don’t excrete enough (often from genetics, medications like diuretics, or kidney disease). Dietary factors (red meat, shellfish, alcohol, fructose) and conditions causing increased cell turnover also contribute.
No. Many people with elevated uric acid never develop gout. However, higher levels and longer duration of hyperuricemia increase risk. Conversely, gout attacks can occur even when uric acid is in the “normal” range.
Limit red meat, organ meats (liver, kidney), shellfish, sardines, and anchovies. Avoid beer and limit spirits. Reduce sugar-sweetened beverages and foods high in fructose. Moderate portions of other meats and fish are generally acceptable.
Yes — beer is worst (contains purines AND blocks excretion), spirits also raise levels, while wine has minimal effect. Alcohol in general impairs kidney uric acid excretion.
Fasting is often recommended as recent food and alcohol intake can affect results. Follow your lab’s instructions.
During an attack, uric acid moves from blood into crystal deposits in the joint, temporarily lowering blood levels. Test again after the attack resolves for accurate baseline.
For gout management: every few months until target achieved, then periodically. For monitoring without gout: annually or as part of metabolic assessment. During cancer treatment at risk for tumor lysis: frequently.
References
Key Sources:
- FitzGerald JD, et al. 2020 American College of Rheumatology Guideline for the Management of Gout. Arthritis Care Res. 2020;72(6):744-760.
- Feig DI, et al. Uric acid and cardiovascular risk. N Engl J Med. 2008;359(17):1811-1821.
- Johnson RJ, et al. Hyperuricemia, acute and chronic kidney disease, hypertension, and cardiovascular disease. Clin J Am Soc Nephrol. 2018;13(8):1273-1280.
