Uric acid builds up in your body when you produce too much of it, excrete too little of it through your kidneys, or both. Normal levels sit around 5.0 mg/dL for men and 4.0 mg/dL for women, and anything above 7.0 mg/dL is considered hyperuricemia. The causes range from diet and alcohol to genetics, medications, and underlying health conditions.
How Your Body Makes Uric Acid
Uric acid is the end product of breaking down purines, compounds that exist naturally in your cells and in the foods you eat. The breakdown happens primarily in the liver, where an enzyme converts purines through a two-step process: first into a compound called xanthine, then into uric acid. This enzyme is the bottleneck of the entire pathway. The faster it works, the more uric acid you produce.
Fat tissue also plays a role. While it doesn’t perform the final conversion step itself, adipose tissue supplies raw materials (specifically hypoxanthine) that the liver then processes into uric acid. This helps explain the well-established link between excess body weight and high uric acid levels.
Why the Kidneys Are Central to the Problem
Your kidneys are supposed to clear uric acid from your blood, but they’re surprisingly reluctant about it. About 98% of uric acid in your blood exists as sodium urate, which passes freely into the kidney’s filtration system. From there, however, your kidneys reabsorb roughly 90% of what they filter, excreting only about 10% in your urine.
This reabsorption happens through a molecular exchange system in the kidney’s proximal tubules. Uric acid swaps places with other small molecules (like lactate and ketone bodies) to move back into the bloodstream. When those other molecules accumulate in higher concentrations, they drive even more uric acid reabsorption, which means less leaves your body. This is exactly what happens during fasting or starvation: rising ketone body levels cause the kidneys to hold onto more uric acid, pushing blood levels higher.
Any condition that reduces kidney function, from chronic kidney disease to dehydration, compromises this already-limited excretion and can trigger a buildup.
Foods That Raise Uric Acid
High-purine foods deliver extra raw material for uric acid production. The biggest offenders are organ meats like liver, kidney, and sweetbreads, which contain some of the highest purine concentrations of any food. Red meat (beef, lamb, pork) contributes moderately, and certain seafood, particularly anchovies, sardines, shellfish, and cod, ranks high as well.
Sugar is a less obvious but significant trigger. Fructose, whether from table sugar or high-fructose corn syrup, is metabolized in the liver by an enzyme that works without any braking mechanism. Unlike glucose metabolism, which has built-in feedback to prevent overconsumption of energy, fructose processing burns through your cells’ energy stores so rapidly that the depleted energy molecules break down into uric acid as a byproduct. This means a can of soda or a bowl of sweetened cereal can spike uric acid through a completely different pathway than a plate of red meat.
How Alcohol Hits You From Both Sides
Alcohol raises uric acid through a double mechanism. First, when your liver metabolizes ethanol, it rapidly consumes energy molecules that then degrade through the same purine breakdown pathway, generating uric acid as a byproduct. Second, the lactic acid produced during alcohol metabolism competes with uric acid for excretion in the kidneys, so less uric acid makes it into your urine.
Beer is the worst offender because it combines both effects with a third: beer itself contains significant amounts of purines from the brewing process. Distilled liquors still raise uric acid through the metabolic pathway but lack the added purine load. Wine appears to carry a lower risk than either beer or spirits, though it isn’t entirely neutral.
Genetics and Uric Acid Transport
Some people are genetically predisposed to high uric acid because their kidneys are less efficient at excreting it. One of the most well-studied examples involves a transporter protein called ABCG2, which sits on the surface of kidney cells and pumps uric acid out into the urine. A common genetic variant reduces this transporter’s capacity by 53%, meaning carriers clear uric acid significantly more slowly than people with the normal version.
This single variant accounts for at least 10% of all gout cases in white populations. A large study of nearly 15,000 people confirmed it as one of the strongest genetic predictors of elevated uric acid. The variant is carried by about 11% of white individuals and 3% of Black individuals. Other genes affecting kidney uric acid transporters have also been identified, and the combined effect of inheriting multiple variants can substantially shift your baseline uric acid level upward regardless of diet or lifestyle.
Medications That Interfere With Excretion
Several commonly prescribed medications raise uric acid levels, usually by reducing how much the kidneys excrete. Diuretics (water pills) are among the most frequent culprits. Both thiazide diuretics, often prescribed for high blood pressure, and loop diuretics used for heart failure cause the kidneys to retain more uric acid. Low-dose aspirin (under 300 mg daily) has the same effect, which is relevant for the millions of people taking a daily baby aspirin for heart protection.
Other medications known to raise uric acid include immunosuppressants used after organ transplants, certain tuberculosis drugs, testosterone therapy, and chemotherapy agents. Chemotherapy can cause a dramatic spike because it kills large numbers of cells rapidly, releasing a flood of purines from the destroyed cells’ DNA all at once.
Health Conditions Linked to Buildup
Several chronic conditions are associated with elevated uric acid, though the relationship often runs in both directions. Kidney disease reduces excretion directly. Metabolic syndrome, diabetes, and fatty liver disease are all tied to higher uric acid levels, likely through a combination of increased production, insulin resistance affecting kidney function, and the fructose metabolism connection. High blood pressure, heart disease, and hypothyroidism also appear on the list of conditions linked to hyperuricemia.
Obesity deserves special mention because it contributes through multiple pathways simultaneously: more adipose tissue supplies more raw materials for uric acid production, insulin resistance impairs kidney excretion, and the dietary patterns associated with weight gain (higher sugar and meat intake) add further fuel.
What Happens When Uric Acid Stays High
When uric acid levels remain elevated over time, the dissolved urate in your blood can crystallize. These needle-shaped crystals deposit most commonly in joints, triggering the intense inflammation known as a gout flare: sudden, severe pain with swelling, redness, and difficulty moving the affected joint. The big toe is the classic location, but gout can strike ankles, knees, wrists, and other joints.
If levels stay high for years without treatment, crystals can accumulate into visible lumps called tophi, hard deposits that form under the skin, in and around joints, and occasionally in organs. Tophi start painless but eventually cause bone erosion, joint deformity, and permanent damage. The kidneys are also vulnerable. High uric acid can lead to kidney stones, and in severe cases, crystal deposits in the kidneys themselves can impair function over time.