It is a heterocyclic compound of carbon, nitrogen, oxygen, and hydrogen with the formula C5H4N4O3.
It forms ions and salts known as acid urates, such as ammonium urate.
Uric acid is a product of the metabolic breakdown of purine nucleotides and is a standard component of urine.
Purines are generated as an end product in digesting specific proteins and DNA in the diet, but some are synthesized in the body.
Uric acid has antioxidant properties but can be pro-oxidant depending on its chemical environment.
Under normal conditions, uric acid is excreted in the urine. However, many factors affect the kidneys’ ability to remove them efficiently. This results in abnormal uric acid levels in the blood (too high or too low).
High blood levels of uric acid can lead to gout and are associated with other medical conditions, such as diabetes and the formation of ammonium urate kidney stones.
In 1776, Swedish chemist Carl Wilhelm Scheele first isolated uric acid from kidney stones. In 1882, the Ukrainian chemist Ivan Horbaczewski first synthesized uric acid by fusing urea with glycine.
Uric acid shows lactim-lactam tautomerism (also often described as keto-enol tautomerism);. However, the lag time form is expected to possess some degree of aromaticity, the uric acid crystallizes into the lactam form, and computational chemistry also indicates that the tautomer is the most stable.
Uric acid is a diprotic acid with pKa1 = 5.4 and pKa2 = 10.3, so it exists predominantly as a monotonic urate ion at physiological pH.
In general, the water solubility of uric acid and its alkali and alkaline earth metal salts is relatively low. These salts exhibit more excellent solubility in hot water than cold water, allowing easy recrystallization.
This low solubility is essential for the etiology of gout. The solubility of the acid and its salts in ethanol is very low or negligible. In ethanol/water mixtures, the solubilities are between the final pure ethanol and pure water values.
Uric acid is the last step in the purine breakdown pathway. The enzyme xanthine oxidase catalyzes the formation of uric acid from xanthine and hypoxanthine, which in turn are produced from other purines.
In simpler terms, purines become hypoxanthine, then xanthine, and finally uric acid.
For the last two steps in the conversion, we need the enzyme xanthine oxidase (uricase). Humans have a mutation that prevents the enzyme production that destroys uric acid (uricase).
Xanthine oxidase is a large enzyme whose active site consists of the metal molybdenum bound to sulfur and oxygen.
Inside cells, xanthine oxidase can exist as xanthine dehydrogenase and xanthine oxidoreductase, which has also been purified from bovine milk and spleen extracts. Uric acid is released under hypoxic conditions.
In humans and higher primates, uric acid (actually hydrogen urate ion) is the end product of oxidation (breakdown) of purine metabolism and is excreted in the urine.
Consequently, humans have higher urate levels (around 240-360 μM) than other mammals (about 30-50 μM in mice).
The enzyme uricase further oxidizes uric acid to allantoin in most other mammals.
The loss of uricase in higher primates parallels the similar loss of the ability to synthesize ascorbic acid, suggesting that urate may partially replace ascorbate in these species.
Both uric acid and ascorbic acid are potent reducing agents (electron donors) and powerful antioxidants. In humans, more than half of the antioxidant capacity of blood plasma comes from the hydrogen urate ion.
The average concentration range for uric acid (or hydrogen urate ion) in human blood is 25 to 80 mg / L for men and 15 to 60 mg / L for women (see below for slightly different values ).
An individual can have serum values as high as 96 mg / L and not have gout. In humans, approximately 70% of the daily elimination of uric acid occurs through the kidneys, and in 5-25% of humans, impaired renal excretion leads to hyperuricemia.
The normal excretion of uric acid in the urine is 250 to 750 mg per day (concentration of 250 to 750 mg / L if one liter of urine is produced per day, higher than the solubility of uric acid because it is in the form of urates dissolved acids).
The Dalmatian dog has a genetic defect in the absorption of uric acid by the liver and kidneys, which decreases the conversion to allantoin, which is why this breed excretes uric acid and not allantoin in the urine.
In birds, reptiles, and some desert-dwelling mammals (e.g., the kangaroo rat), uric acid is also the end product of purine metabolism but is excreted in the feces as a dry mass.
This involves a complex metabolic pathway that is energy expensive compared to processing other nitrogenous wastes such as urea (from the urea cycle) or ammonia but has the advantages of reducing water loss and preventing dehydration.
Platynereis dumerilii, a Polychaete marine worm, uses uric acid as a sex pheromone released into the water by females during mating to induce males to release sperm.
A proportion of people have mutations in the proteins responsible for the excretion of uric acid by the kidneys. So far, variants within several genes have been identified:
- SLC2A9; ABCG2; SLC17A1; SLC22A11; SLC22A12; SLC16A9; GCKR; LRRC16A; and PDZK1. SLC2A9 is known to transport uric acid and fructose.
Clinical importance and research
In human blood plasma, the reference range for uric acid is typically 3.4-7.2 mg / dL (200-430 μmol / L) for men, and 2.4-6.1 mg / dL for women (140-360 μmol / L ) – one milligram per deciliter (mg / dL) is equal to 59.48 micromoles / liter (μmol / L).
In blood plasma above and below the normal range, uric acid concentrations are known as hyperuricemia and hypouricemia, respectively.
Similarly, below-average uric acid concentrations are known as hyperuricosuria and hypouricosuria. Uric acid levels in saliva may be associated with uric acid levels in the blood.
High uric acid
An excess of uric acid in the body is known as hyperuricemia.
Diet can be a factor. High intakes of dietary purine, high fructose corn syrup, and table sugar can increase uric acid levels. Serum uric acid can be elevated by reduced excretion through the kidneys.
Rapid or fast weight loss can temporarily raise uric acid levels. Certain medications, such as thiazide diuretics, can increase uric acid levels in the blood by interfering with renal clearance.
Tumor lysis syndrome is a metabolic complication of certain cancers or chemotherapy due to the release of nucleobases and potassium in plasma.
High uric acid levels have been linked to:
- Kidney stones
- High blood pressure
- Kidney disease
- Cognitive dysfunction.
Diseases associated with high uric acid
Urates are found in urine, blood, and tissue. Urate deposits can cause oxidative stress, inflammation, and cellular (endothelial) dysfunction.
People with high uric acid without symptoms generally don’t need any medical treatment, but it does pose several health risks, so high uric acid levels need to be addressed.
High uric acid levels lead to gout.
Hyperuricemia (high uric acid levels), which induces gout, has several potential origins.
A gout is a form of inflammatory arthritis associated with hyperuricemia. It occurs when there are high uric acid levels in the circulating blood, which causes needle-like crystals of uric acid to precipitate in the joints, capillaries, skin, and other tissues.
Symptoms appear suddenly, overnight. It comes with unbearable pain, redness, and swelling of the joint. Too much food, alcohol, starting a diuretic, or dehydration can precip the attack.
Symptoms go away after 10-15 days, but they can keep returning. Over time, stone-like deposits known as tophus can build up in joints, ligaments, and tendons, leading to possible joint deformation.
Gout can occur when serum uric acid levels are as low as 6 mg / dL (~ 357 μmol / L), but an individual can have serum values as high as 9.6 mg / dL (~ 565 μmol / L) and not have gout.
In humans, purines are metabolized to uric acid, which is then excreted in the urine. Consuming some types of foods rich in purines, especially meat and seafood, increases the risk of gout.
Gout can arise from the regular consumption of meats, such as liver, kidney, and gizzards, and certain types of shellfish such as anchovies, herring, sardines, mussels, scallops, trout, haddock, mackerel, and tuna.
However, moderate intake of purine-rich vegetables is not associated with an increased risk of gout. Treatment for gout in the 19th century was the administration of lithium salts; lithium urate is more soluble.
Currently, inflammation during attacks is most often treated with non-steroidal anti-inflammatory drugs (NSAIDs), colchicine, or corticosteroids, and urate levels are controlled with allopurinol.
Allopurinol, which weakly inhibits xanthine oxidase, is a hypoxanthine analog hydroxylated by xanthine oxidoreductase at position 2 to give oxypurinol.
Tumor lysis syndrome
Tumor lysis syndrome, an emergency condition that can result from blood cancers, produces elevated uric acid levels when tumor cells release their contents into the blood, either spontaneously or after chemotherapy.
Tumor lysis syndrome can lead to acute kidney failure when uric acid crystals deposit in the kidneys.
Treatment includes hyperhydration to dilute and excrete uric acid through the urine, rasburicase to reduce poorly soluble uric acid levels in the blood, or allopurinol to inhibit purine catabolism increase uric acid levels.
Hyperuricemia is caused by Lesch-Nyhan syndrome.
Lesch-Nyhan syndrome, a sporadic genetic disorder, is also associated with elevated serum uric acid levels in the blood.
In this syndrome, spasticity, muscle stiffness, involuntary movement, self-injury, cognitive delay, and the formation of gout are present in cases of this syndrome and manifestations of gout.
In Lesch-Nyhan syndrome, hypoxanthine-guanine phosphoribosyltransferase (HPRT), an enzyme involved in purine nucleotide recycling, is mutated.
This leads to increased uric acid production because the purine nucleotides cannot be reused, so they are subsequently degraded.
High uric acid levels lead to metabolic syndrome.
Blood uric acid is significantly correlated with metabolic syndrome and its components, particularly blood triglycerides and waist circumference.
This could have to do with the high fructose intake in soft drinks and processed foods that raise uric acid levels and cause insulin resistance and obesity.
This may also be because increased uric acid after fructose intake induces insulin resistance (by lowering nitric oxide), a key factor involved in metabolic syndrome.
High uric acid is associated with hypertension and chronic kidney disease.
Hyperuricemia is associated with hypertension (HTN) and chronic kidney disease (CKD).
Hyperuricemia can increase risk factors for cardiovascular disease. In rats, hypertension associated with a high uric acid level was reversible with drugs that reduce uric acids, such as febuxostat and allopurinol.
Hypertension and chronic kidney disease are associated with an increased risk of heart and metabolic disorders.
These include hardening of the arteries, heart failure, stroke, type 2 diabetes, metabolic syndrome, nonalcoholic fatty liver disease, etc.
Uric acid can damage blood vessels, increase oxidative stress, and cause platelets and red blood cells to stick together. These increase the risks of adverse cardiac events.
Chronic hyperuricemia in gout patients increases uric acid crystal accumulation in kidney tissues, resulting in tissue damage and inflammation.
Hyperuricemia is linked to type 2 diabetes.
Uric acid in the blood is associated with an increased risk of type 2 diabetes, regardless of obesity, high cholesterol, and blood pressure.
Hyperuricemia may be a consequence of insulin resistance in diabetes rather than its precursor.
Hyperuricemia is believed to increase the risk of diabetes by increasing oxidative stress and inflammation (by increasing tumor necrosis factor-alpha), both factors related to the development of diabetes.
One study showed that high serum uric acid was associated with an increased risk of type 2 diabetes, regardless of obesity, dyslipidemia, and hypertension. Hyperuricemia is associated with components of metabolic syndrome, even in children.
High uric acid increases the risk of kidney stones.
If your urine contains more calcium, oxalate, and uric acid, you will develop kidney stones. Kidney stones can form through deposits of sodium urate microcrystals.
Saturated levels of uric acid in the blood can lead to the form of kidney stones when urate crystallizes in the kidney. These uric acid stones are radiolucent and do not appear on a plain abdominal X-ray.
Uric acid crystals can also promote calcium oxalate stone formation, acting as “seed crystals.”
The most common risk factor for uric acid stones is acidic urine (pH <5.5) because uric acid stones precipitate in acidic environments. Therefore, patients should increase their alkaline load by eating more fruits and vegetables.
Uric acid levels are elevated in Down syndrome.
Down syndrome patients consistently have higher levels of uric acid in their blood.
High uric acid levels can increase the risk of bone fracture.
Increased urate levels in the blood are associated with an increased risk of hip fractures in men.
High uric acid levels induce inflammation in bone, affect nitric oxide availability, and suppress vitamin D activation, increasing bone fragility and the risk of fractures.
Hyperuricemia is related to erectile dysfunction.
Erectile dysfunction is commonly seen in gout patients.
This is likely because high uric acid levels are strongly linked to poor blood vessel function, hypertension, and microvascular disease (disease of the smallest blood vessels), risk factors for erectile dysfunction.
Blood uric acid levels were significantly higher in psoriasis patients compared to controls.
However, uric acid levels did not increase or decrease the inflammation observed in these patients.
Causes of high uric acid
Kidney problems increase uric acid levels.
The highest uric acid levels occur when the kidneys do not remove them efficiently. This could be due to kidney dysfunction and the influence of specific metabolites and medications.
High protein diets increase uric acid levels.
Studies have shown that each additional serving of meat per day increases the risk of gout by 21%.
In a crossover study design, the effect of eating some foods rich in purines, such as beef liver, haddock fillets, and soybeans, was investigated. The results showed that ingestion of all the test meals caused an increase in uric acid levels in the blood.
Fructose increases uric acid levels.
The high dietary intake of fructose in foods and beverages increases the production of inosine and purines. Additionally, fructose competes with uric acid for secretion in the kidney.
Fructose rapidly increases uric acid levels because it activates enzymes that break down adenosine triphosphate into monophosphate (fructokinase and adenosine deaminase), leading to increased activity in inosine production.
In addition, fructose stimulates uric acid synthesis from amino acid precursors, such as glycine.
Diuretics increase uric acid levels
Diuretics are one of the most important causes of secondary hyperuricemia. The drugs increase uric acid levels in the blood by increasing uric acid reabsorption and decreasing uric acid secretion.
Alcohol increases uric acid levels
According to a population-based cohort study, alcohol-related illnesses were significantly associated with the risk of gout. Furthermore, severely alcohol-dependent patients were associated with an increased risk of gout.
Alcohol can stimulate uric acid production by increasing lactic acid, reducing uric acid excretion in the kidneys.
Additionally, alcohol accelerates the breakdown of purines, which increases uric acid production.
Hypothyroidism increases uric acid levels.
Hyperuricemia and gout are frequently found in patients with hypothyroidism.
Thyroid hormones (T4 and T3) stimulate energy production processes, and their deficiency affects purine metabolism, resulting in increases in uric acid levels and hyperuricemia.
Additionally, hypothyroidism can reduce kidney blood flow and filtration rate, which raises uric acid levels in the blood.
Obesity increases uric acid levels
According to a population-based epidemiological study, obesity increases the risk of developing hyperuricemia. If you are overweight, your body makes more uric acid. As a result, the kidney has a more challenging time getting rid of uric acid.
Blood uric acid levels correlate with leptin levels. Since obese people have higher leptin levels (due to leptin resistance), high leptin may be related to the development of hyperuricemia in obesity.
Genes that increase uric acid levels
Your genes influence uric acid levels. The UCP2 gene controls the urate concentration in the blood and the risk of hyperuricemia. The degree of association varies with gender and body mass index (BMI) levels.
In addition, mutations in the secretory urate transporter genes, SLC2A9, ABCG2, SLC17A1, or SLC17A3, can cause hyperuricemia.
Male sex and sex hormones
Men have higher uric acid levels in their blood than women and are at a higher risk of developing gout.
Estrogen is required for the regular elimination of urate through the kidneys. During the postmenopausal period, women have the same uric acid content as men of similar age, suggesting that low estrogen may play a role in developing hyperuricemia.
The uric acid content in the blood increases with age. In addition, the prevalence of gout increases approximately four times to 4.1% by the age of 75 years.
Vitamin D deficiency is significantly correlated with hyperuricemia in postmenopausal women.
Ketogenic diet and high sodium intake
A ketogenic diet reduces the kidney’s ability to excrete uric acid due to competition for transport between uric acid and ketones. Higher sodium intake is associated with increased uric acid levels in the blood.
Elevated levels of parathyroid hormone in the blood are associated with higher levels of uric acid in the blood in the general population. Although the exact mechanisms are unclear, it is believed that the parathyroid hormone increases uric acid in the blood by reducing the excretion of urate in the kidney.
Chronic lead poisoning leads to hyperuricemia.
Exposure to lead is associated with impaired kidney function and increased uric acid levels in the blood.
High levels of lead damage the kidneys, cause inflammation, and inhibit urate excretion, resulting in the accumulation of urate and eventually saturnine gout (i.e., lead drop).
- Immunosuppressive drugs.
How to lower uric acid naturally.
Weight loss can help reduce high uric acid levels in overweight and obese people.
Purine restricted diet
Avoid alcohol, red meat, seafood, and sugary drinks. Avoid/limit refined carbohydrates if you have high uric acid levels. The lowest-purine foods include eggs, fruits, cheese, nuts, and vegetables other than legumes.
Dehydration leads to elevated uric acid levels.
Vitamin C increases uric acid excretion in the urine and thus reduces uric acid levels in the blood.
Caffeine is a methylxanthine and can be a competitive inhibitor of xanthine oxidase. However, a study compared the effects of coffee, tea, and caffeine intake on uric acid levels.
It found that coffee consumption was associated with lower uric acid levels due to components of coffee other than caffeine, suggesting that non-caffeinated coffee (regular or decaffeinated) is responsible for the reverse association.
Milk proteins (i.e., casein and lactalbumin) promote uric acid excretion in the urine.
Cherries lower uric acid levels in the blood by increasing kidney filtration rate and decreasing uric acid reabsorption. Cherries are also natural xanthine oxidase inhibitors.
Medical treatments to reduce uric acid
Non-steroidal anti-inflammatory drugs
Most non-steroidal anti-inflammatory drugs increase urinary uric acid excretion and are recommended to treat gout.
These drugs increase the uric acid secretion in the urine: probenecid, sulfinpyrazone, and benzbromarone.
Uricosuric drugs generally prevent the kidney from absorbing uric acid back into the blood (blocking the function of URAT1).
Xanthine Oxidase Inhibitors
Allopurinol is recommended because it prevents gout, but it is also taken when patients have a particular form of leukemia or lymphoma to prevent a complication of chemotherapy or tumor lysis syndrome.
Furthermore, allopurinol is currently not indicated in asymptomatic hyperuricemia and related heart disease or diseases other than gout due to its adverse effect.
Febuxostat is a selective xanthine oxidase/xanthine dehydrogenase inhibitor.
It has several advantages over allopurinol, including tolerability in patients with hypersensitivity to allopurinol, more efficacy in renal failure, and faster dissolution of tophi.
Febuxostat works quickly, and treatment usually begins at a dose of 40 mg/day. If the uric acid level in the blood does not drop to 6.0 mg / dL in two weeks, the dose can be increased to 80 mg/day.
The average reduction in uric acid level in the blood is 40% and 56% at 40 mg/day and 80 mg/day, respectively, and is similar in individuals with and without renal failure, in contrast to allopurinol.
Low uric acid
Low uric acid ( hypouricemia ) can have many causes. Low dietary zinc intakes cause lower uric acid levels. This effect can be even more pronounced in women taking oral contraceptive drugs.
Sevelamer, a drug indicated to prevent hyperphosphatemia in people with chronic kidney disease, can significantly reduce serum uric acid.
Blood uric acid levels are considered low (hypouricemia) at 2 mg/dl or less. It is not considered a medical condition but rather a helpful medical sign.
Uric acid is lower in multiple sclerosis, Parkinson’s disease, motor neuron disease, Alzheimer’s disease, and Huntington’s disease.
Lower blood values have been associated with several disorders of the nervous system. It has been proposed that higher uric acid levels in the blood may be neuroprotective.
In a large population-based cohort study, a negative relationship between gout and Parkinson’s disease was observed in patients 65 years of age and older.
A similar trend has been shown between uric levels and Huntington’s disease, suggesting that uric acid may play a role in preventing neurodegeneration.
The meta-analysis of 10 case-control studies found that the serum uric acid levels of multiple sclerosis patients were significantly lower than healthy controls, possibly indicating a diagnostic biomarker for multiple sclerosis.
Uric acid is reduced in optic neuritis.
Uric acid levels are lower in patients with optic neuritis, an inflammatory demyelinating disease of the optic nerve that is often the first symptom of multiple sclerosis.
Wilson’s disease can lead to low uric acid levels.
Wilson’s disease is a disease in which copper accumulates in the tissues of vital organs such as the brain and liver.
It can decrease uric acid levels in the blood due to associated kidney problems (i.e., Fanconi syndrome) that increase urinary uric acid excretion.
Normalize low uric acid
Correcting low zinc levels can help raise the serum uric acid level.
What Causes Low Uric Acid Levels?
Medication / treatments
Hypouricemia can be found in 1% of hospitalized patients. In most cases, the cause is related to medications such as salicylates, allopurinol, X-ray contrast agents, and glyceryl guaiaclate.
In addition, medications such as losartan (an angiotensin II receptor antagonist drug), fenofibrate (drug in the fibrate class, used primarily to lower cholesterol levels), and some non-steroidal anti-inflammatory drugs lower serum uric acid levels.
In addition, forced diuresis (increased urination) used primarily in treating renal colic (abdominal pain from kidney stones) in suicide attempt patients can lead to hypouricemia.
Your genes influence uric acid levels. The two kidney urate transporters are human urate transporter 1 (URAT 1) and human glucose transporter-like protein 9 (GLUT 9).
A genetic mutation in these two transporters is responsible for idiopathic hypouricemia.
The SLC2A9 gene encodes a protein that helps transport uric acid in the kidney. Variants of this gene are known to have significant associations with uric acid in the blood.
Several malignancies such as Hodgkin’s disease, sarcoma, glioblastoma, and various carcinomas have been associated with hypouricemia.
By following a low-purine diet, uric acid levels can be reduced by only 15%.
Mineral intake / deficiency
In a case study of molybdenum deficiency, blood hypouricemia was present.
Inadequate zinc intake in the diet can lead to lower uric acid levels. This effect is more common in women taking oral contraceptives. Patients with high copper/iron levels experience hypouricemia.
Magnesium intake is correlated with a lower likelihood of high uric acid levels in men. This could be due to the laxative effect of magnesium, which may play a potential role in increasing uric acid excretion.
Estrogen suppresses the protein production that removes urate in the kidney (organic anion transporter of proximal tubule epithelial cells), while androgens stimulate it. This explains the lower serum urate levels in postmenopausal women compared to men.
Blood test for uric acid
A blood uric acid test, also known as a serum uric acid measurement, determines the amount of uric acid present in the blood. The test can help determine how well your body makes and removes uric acid.
Purposes of a uric acid blood test
A uric acid blood test is the most common test used to:
- Diagnose and monitor people with gout.
- Monitor people who are undergoing chemotherapy or radiation therapy.
- Monitor kidney functions after injury.
- Find the cause of kidney stones.
- Diagnose kidney disorders.
Preparing for a uric acid blood test
The following can interfere with the results of your uric acid test:
- Certain medications
- High levels of vitamin C.
- Dyes are used in X-ray tests.
Tell your doctor about any prescription or over-the-counter medications you are taking.
You may need to fast (refrain from eating or drinking) for four hours before the test.
How a uric acid blood test is done
The process of obtaining a blood sample for testing is called venipuncture.
Your doctor or other healthcare provider draws blood from a vein, usually from your inner elbow or the back of your hand. First, they sterilize the area with an antiseptic. They then wrap an elastic band around your arm to allow the blood to fill the veins.
They then insert a needle into your vein. The blood is collected in an attached vial. Once the blood has been collected, the plastic band is untied, and the hand is removed from the vein. Pressure is applied to the needle entry site, and a bandage is used if necessary.
A small cut may be made in the arm for infants and young children, and a test strip or slide may be made to collect a small blood sample. The area is cleaned and bandaged if necessary.
Once collected, the blood is sent to a laboratory for analysis.
What the test results mean
Uric acid levels can vary by gender.
Guideline values for blood uric acid levels generally fall between 2.6 – 5.7 milligrams/deciliter (mg / dL) for women and 4.0 to 8.5 mg / dL for men, although this can vary between laboratories.
It is also possible to have too little uric acid in your blood, a liver or kidney disease symptom. It is also a symptom of Fanconi syndrome, a kidney tubule disorder that prevents the absorption of substances such as glucose and uric acid.
The uric acid blood test is not considered a definitive test for gout.
Only testing a person’s joint fluid for monosodium urate can confirm the presence of gout. However, your doctor may make an educated guess based on high blood levels and your gout symptoms.
Also, it is possible to have high uric acid levels without gout symptoms. This is known as asymptomatic hyperuricemia.
Urine test for uric acid
A uric acid test measures the amount of uric acid in the body. A uric acid test is often done to help determine the underlying cause of abnormal uric acid levels.
By measuring the amount of uric acid in your body, your doctor can assess how well your body produces and removes uric acid. Your doctor may perform a uric acid blood test, or they may test your uric acid with a urine sample.
Why is a uric acid urine test done?
Your doctor will usually recommend a uric acid urine test when you show symptoms of a medical condition that causes uric acid levels to rise.
An increased amount of uric acid in the urine often indicates gout, a common form of arthritis. This condition is characterized by severe pain and tenderness in the joints, especially the toes and ankles. Other symptoms of gout include:
- Swelling in a joint
- Red or discolored skin around a joint.
- A joint that is hot to the touch.
Your doctor may order a urine test to determine how well you recover from kidney stones or gout.
A uric acid urine test may also monitor your condition if undergoing chemotherapy or radiation therapy. These treatments can lead to a buildup of uric acid in the body.
How do I prepare for a uric acid urine test?
It is important to tell your doctor about any prescription drugs, over-the-counter drugs, or supplements you are taking before having a uric acid urine test.
Certain medications can affect the accuracy of this test, such as aspirin (Bufferin), ibuprofen (Advil), and water pills. Your doctor may instruct you to stop taking these medications before the test.
Your doctor may also ask you to refrain from drinking alcohol immediately before and during the test.
How is a uric acid urine test performed?
A uric acid urine test is a safe and painless procedure that only requires urine collection. Urine samples must be collected over 24 hours. Your doctor will explain how to manage your urine correctly.
The urine collection procedure is as follows:
On day 1, urinate in the bathroom after waking up. Wash this sample first. After that, note the time and collect all the urine for the remaining 24 hours. Store urine samples in a refrigerator or other cool place.
Return the containers to the appropriate person as soon as possible. It is essential to wash your hands carefully before and after collecting each urine sample. Be sure to cover the containers tightly and label their containers.
Once the samples have been collected, the urine is sent to a laboratory for analysis. The results will be delivered to your doctor within a few days. Your doctor will discuss your results with you and explain what they mean in more detail.
Normal results for this test are:
- Adults (normal diet): 250-800 mg / day.
- Adults (purine-free diet): <420 mg / day.
- Adults (low purine diet): <480 mg / day in men and <400 mg / day in women.
- Adults (high purine diet): <1000 mg / day.
Diet, exercise, and other healthy lifestyle changes can improve gout and other diseases caused by high uric acid levels. However, they cannot always replace necessary medical treatment.
Take all prescription medications as directed by your doctor. The right combination of diet, exercise, and medications can help keep symptoms at bay.
It may seem like many foods you should avoid to help lower uric acid levels. The best way to limit these foods is by making a weekly meal plan. Talk to your dietitian to help you make the best diet plan.
Keep a list of foods on your shopping list that you must eat rather than what you cannot eat. Stick to the list while shopping at the grocery store.
You can also join an online support group for people with uric acid-related illnesses to get more ideas on preparing the best meals for yourself.