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If you have ever had a kidney stone or been told your uric acid is high, this test can answer a question that a standard blood draw cannot: is the problem overproduction or under-excretion? Your blood level of uric acid tells you how much is circulating. Your 24-hour urinary uric acid tells you how much your body is actually getting rid of. That distinction matters because it changes what you do next.
24-hour urinary uric acid measures the total amount of uric acid your kidneys filter into your urine over a full day. Uric acid is the end product of purine metabolism, the process your body uses to break down purines, molecules found in every cell and in many foods. When cells turn over or when you eat purine-rich foods, uric acid is produced, and most of it is cleared through the kidneys.
The normal range is generally considered to be below 800 mg per day for men and below 750 mg per day for women. When excretion exceeds these thresholds, the condition is called hyperuricosuria, and it raises the risk of forming both uric acid kidney stones and calcium oxalate stones. But a single collection can be misleading: even in healthy people, about 20.7% of measurements temporarily exceed 800 mg per day, which is why repeat testing is important.
Your kidneys do the majority of the work, clearing roughly 60 to 70% of the uric acid your body produces. The rest is handled by cells lining your intestines. But the kidney's process is not a simple filter. Nearly all the uric acid that passes through your kidney's filtration system is reabsorbed back into the blood. About half is then secreted again into the urine, only to be partially reabsorbed once more. The net result is that only about 10% of the filtered uric acid actually leaves your body in urine.
This tug of war between reabsorption and secretion is controlled by a set of specialized transport proteins sitting on the surface of kidney cells. The most important ones include URAT1 (a reabsorption channel), GLUT9 (which moves uric acid in both directions), and ABCG2 (which pushes uric acid out into both the urine and the intestine). Genetic variations in any of these transporters can shift your baseline excretion significantly.
This is not a routine screening test. It is most useful in specific clinical scenarios where knowing how much uric acid you excrete changes a decision.
It is worth noting that the 2020 American College of Rheumatology gout guidelines conditionally recommend against routine urinary uric acid testing before starting uricosuric therapy, citing the practical difficulty of a full 24-hour urine collection and limited evidence. However, the same guidelines acknowledge that higher 24-hour urinary uric acid levels are associated with kidney stones, and they advise against using uricosuric drugs in anyone with known kidney stones or moderate to severe chronic kidney disease.
Your urinary uric acid level is influenced by what you eat, what medications you take, and how well your kidneys function. Understanding these factors helps you interpret your result and identify what you can change.
Diet is one of the most modifiable drivers. Foods high in purines, including organ meats, red meat, seafood, and dried beans, directly increase uric acid production and excretion. Alcohol has a double effect: it increases uric acid production while also impairing excretion, and beer adds purines on top of that. Fructose and high-fructose corn syrup trigger a specific metabolic pathway that accelerates purine breakdown, raising uric acid output.
Body composition matters too. Higher BMI is associated with increased urinary uric acid excretion in observational studies of healthy adults. This appears to reflect both greater purine turnover from a larger body mass and the metabolic changes that accompany excess weight.
Medications can push this number in either direction. Uricosuric drugs like probenecid, lesinurad, and benzbromarone are designed to increase urinary uric acid. Losartan (a blood pressure medication) and fenofibrate (a cholesterol drug) have mild uricosuric effects as well. On the other side, thiazide and loop diuretics tend to decrease uric acid excretion by causing volume contraction and altering transporter activity. Pyrazinamide, ethambutol, niacin, and cyclosporine also reduce excretion.
Kidney function is a major determinant. Higher estimated glomerular filtration rate (eGFR), which reflects how well your kidneys filter, is associated with higher urinary uric acid excretion. Chronic kidney disease reduces the filtered load and lowers excretion. If your kidney function is impaired, a "normal" urinary uric acid level may mask true overproduction because your kidneys simply cannot clear it fast enough.
Metabolic syndrome and insulin resistance deserve special mention. When insulin levels are chronically elevated, the kidney ramps up its reabsorption of uric acid through the URAT1 and GLUT9 transporters while simultaneously reducing secretion through ABCG2. The net effect is decreased urinary excretion and rising blood levels. This means that in people with metabolic syndrome or type 2 diabetes, urinary uric acid may appear normal or low even while serum uric acid climbs.
What this means for you: if you are trying to lower your urinary uric acid, the most accessible steps are reducing purine-rich foods, cutting back on alcohol (especially beer), and minimizing fructose intake. If you are on a medication that affects uric acid handling, discuss the tradeoffs with your clinician. And if you have insulin resistance, understand that your urinary result needs to be interpreted alongside your blood level and kidney function to get the full picture.
Before looking at your number, consider your kidney function. If your eGFR is reduced, your urinary uric acid may be artificially low because your kidneys are not filtering efficiently. In that setting, even a "normal" excretion value does not rule out overproduction.
| Excretion Level | What It Suggests | Likely Next Step |
|---|---|---|
| Below 600 mg/day | Your kidneys may not be excreting enough uric acid, especially if your blood level is high. This pattern points toward underexcretion as the cause of hyperuricemia. | Focus on whether medications, kidney disease, or insulin resistance are limiting excretion. |
| 600 to 800 mg/day (men) or 600 to 750 mg/day (women) | Within the typical range. If your blood uric acid is also normal, purine metabolism is likely balanced. | No specific action needed unless you have other risk factors for kidney stones. |
| Above 800 mg/day (men) or above 750 mg/day (women) | Hyperuricosuria. Your body is excreting more uric acid than usual, which raises the risk of uric acid and calcium oxalate stones. | Evaluate dietary purine intake, check for conditions causing high cell turnover, and discuss stone prevention strategies. |
What this means for you: a single high result does not necessarily mean you have a chronic problem. Transient hyperuricosuria is common. If your first collection comes back elevated, repeating the test on a different day with your usual diet gives a more reliable picture.
The 24-hour collection correlates strongly with serum urate levels (correlation coefficient of 0.928), making it the most reliable urinary measure for assessing purine metabolism. A spot urine alternative exists: the random urine uric acid to creatinine ratio, which shows a moderate correlation (r = 0.398) with the 24-hour value. It is less precise but may be useful as a screening tool when a full day collection is impractical.
Certain lab factors can occasionally affect the result, so ensure your collection is complete and properly stored according to the lab's instructions.