Most uric acid dissolves in your blood, then goes to the kidneys. From there, it leaves the body through your urine. If your body makes too much uric acid or doesn't release enough into your urine, it can make crystals that form in your joints. This condition is known as gout. Gout is a form of arthritis that causes painful inflammation in and around the joints.
High uric acid levels can also cause other disorders, including kidney stones and kidney failure. In addition, you may need this test if you are undergoing chemotherapy or radiation therapy for cancer. These treatments can raise uric acid levels. The test can help make sure you get treated before levels get too high. During a blood test, a health care professional will take a blood sample from a vein in your arm, using a small needle.
After the needle is inserted, a small amount of blood will be collected into a test tube or vial. You may feel a little sting when the needle goes in or out. This usually takes less than five minutes. For a uric acid urine test, you'll need to collect all urine passed in a hour period. This is called a hour urine sample test. Your health care provider or a laboratory professional will give you a container to collect your urine and instructions on how to collect and store your samples.
A hour urine sample test generally includes the following steps:. You don't need any special preparations for a uric acid blood test.
Be sure to carefully follow all the instructions for providing a hour urine sample. Low levels of uric acid in blood are uncommon and not usually cause for concern.
Low levels of uric acid in urine can be a sign of kidney disease, lead poisoning , or heavy alcohol use. There are treatments that can reduce or raise uric acid levels. This mixture of quantitative and qualitative etiological hyperuricemia factors is confounding because normouricemic individuals may show symptoms while others with hyperuricemia may not. In the clinical context, hyperuricemia is seen as a prognostic indicator of renal disease, diabetes mellitus, cardiovascular disease and inflammation [ 7 , 17 - 23 ], thus being a modest risk factor for mortality [ 1 ].
Physiologically, uric acid plasma concentrations increases with age; they are smaller in women of childbearing age and, in post menopause women, it increase to similar values to those found in males [ 2 , 3 ]. Uric acid entry into the pool is controlled by hepatic production, which receives endogenous nucleoproteins and exogenous dietary precursor proteins.
Uric acid exit from the pool in males is mainly controlled by the kidneys and by urine-forming factors, renal plasma flow, glomerular filtration and tubular exchange [ 24 , 25 ]. In the kidney, uric acid and urate are initially filtered and additionally secreted. The factors that can influence the uptake of urate by the kidney are: plasma concentrations, volemia and renal plasma flow modulators. At this point, renal excretion of urate follows the same extra-renal limiting factors as those of glomerular filtration.
In this phase, the renal excretion of urate follows the limiting factors that accompany renal diseases glomerular and medullary. The urate renal excretion phase is that of post-secretory resorption [ 24 ]. Proximal tubular reabsorption of uric acid is competitive with monocarboxylic organic acids, and it can be inhibited by oxalic acid, lactic acid and ketone bodies acetoacetic and beta-hydroxybutyric acids. Metabolic situations with higher production and circulation of such acids are accompanied by the hypoexcretion of uric acid in urine [ 24 ].
Ketone bodies are produced in the liver by partial oxidation of acetyl coenzyme A due to excessive peripheral lipolysis. Ketonuria occurs in decompensated diabetic individuals and in acute fasting weight loss by carbohydrate-restricted diets. Factors that increase uric acid urinary excretion: extracellular volume expansion and tubular resorption inhibition [ 24 ].
Acute renal failure can also rise UA by decreased of renal excretion [ 26 ]. Furthermore, the consumption of some drugs are associated with the raise of serum UA ciclosporin, ethambutol, pyrazinamide, cytotoxic chemotherapy. On the other hand, other drugs benzbromarone, losartan, probenecid, sulfinpyrazon diminishes the UA concentration mainly by the inhibition of a specific anion transporters URAT1 , that is responsible for the reabsorption of renal uric acid, which explain the uricosuric effect of these drugs [ 2 ].
Purine bases and their nucleotides are rapidly captured by the liver [ 27 ] and converted into xanthines, metabolized by uric acid or recycled by salvage pathways or de novo synthesis, and the latter requires a higher energetic cost ATP consumption [ 28 ]. Uric acid formation by xanthine occurs via hypoxanthine by the action of xanthine oxidase [ 29 ]. In most mammals, uric acid is converted into allantoin by uricase and later into urea, which are excreted. Diseases accompanied by great cell depletion, such as leukemia, leukocytosis and dystrophies can increase the provision of nucleic acids to the liver and result in a larger production of uric acid.
Hence, diseases resulting from innate purine metabolic errors may also result in hyperuricemia [ 2 , 3 , 12 ]. The relation between diet and UA has not yet been fully clarified since most studies have not estimated basal urate concentrations, have not excluded confounding factors or have not even correctly evaluated ingested nutrients [ 32 ].
The human diet is very poor in urate, which is produced mainly in the liver and to a less extent in the small intestine.
It is recommended that individuals with hyperuricemia should not ingest a large amount of purine-rich food for instance, veal, bacon, kid meat, mutton, turkey, pork, duck, goose, etc. During fructose metabolism, the phosphorylation of such monosaccharide into fructose 1-phosphate occurs by means of enzyme fructokinase.
When high fructose intake occurs, fructose phosphorylation into fructose 1-phosphate is fast, but the reaction with aldolase is slow. Hence, fructose 1-phosphate accumulates, and inorganic concentrations of intracellular phosphate also decrease. There are other ways to increase urate concentrations, such as the intake of sorbitol, sucrose, lactate and methylxanthines [ 38 ].
After absorption, sorbitol is converted into fructose by the liver, and thus, it can increase UA production [ 39 , 40 ]. Fruit and vegetables, in addition to flavonoids, can contain other nutrients that can affect the plasma total antioxidant capacity TAC. The mechanism for such elevation would be the degradation of purine nucleotides or UA excretion reduction [ 41 - 43 ]. High vitamin-C intake shows an inverse relation with UA [ 44 ] as such vitamin has a uricosuric effect due to competition of UA renal resorption through a change in the anion transportation system in the proximal tubule [ 45 , 46 ].
Beer intake is an independent factor from UA increase [ 32 ] both due to its alcoholic content and high-quality purine [ 47 ].
Beer intake has a stronger power to increase UA than liqueur, but moderate wine intake does not increase UA [ 36 , 48 ]. Alcohol intake increases UA concentrations by reducing excretion [ 49 , 50 ] and increasing urate production [ 51 ]. Dairy product intake has an inverse relation with UA [ 32 , 36 , 52 ]. Probably, the mechanism for such association is due to milk-forming proteins lactalbumin and casein , which have a uricosuric effect [ 53 ].
There is an inverse relation between coffee intake and UA concentrations [ 48 ], but such association seems to be due to other substances, as it does not seem to result from caffeine. Decreased UA concentrations would result from the improved insulin resistance observed with increased coffee intake, which occurs mainly due to chlorogenic acid, an antioxidant found in that drink [ 54 , 55 ].
Tsunoda et al. This type of diet indirectly decreased UA serum concentrations because it improved insulin sensitivity in these individuals, and this occurred regardless of changes in body weight or blood pressure. Gout is caused by articulation deposition of monosodium urate crystals after chronic hyperuricemia [ 2 ]. Uric acid values higher than 7. Renal calculi are formed by calcium salts deposited on an organic matrix of oxalate or urate. Their formation occurs in the glomerular filtrate in acid oxalate or urate or alkaline carbonates and phosphates pH in the presence of high calciuria hyperparathyroidism or bone demineralization.
They are usually formed and then dissolved, but under abnormal pH variation or filtrate concentration conditions, they may remain until excretion [ 30 ]. The contribution of UA to renal stone formation has an important role in progressive renal failure [ 57 ]. Meta-analysis has recently shown that UA elevation is related to an increase in coronary artery disease infarction and mortality events [ 1 ], and epidemiological studies showed that UA is an independent risk factor for cardiovascular diseases [ 5 , 10 ], particularly in hypertensive and diabetic individuals [ 21 ].
It is also speculated that UA is one of the determinants of the metabolic syndrome [ 22 ]. Individuals with high UA levels have an odds ratio of 1. UA is associated with Metabolic Syndrome [ 59 ] and its components [ 60 ], obesity, dyslipidemia, hypertension [ 18 ], insulin resistance metabolic syndrome , increased C-reactive protein PCR concentration [ 23 ] and endothelial dysfunction [ 20 ], or even, to risk factors for cardiovascular diseases [ 7 , 17 , 19 ].
UA increase is observed in individuals with insulin resistance, probably because hyperisulinemia would cause lower renal UA excretion [ 61 ]. Additionally, insulin could indirectly act on UA, since there is an association between hyperinsulinemia and hypertriglyceridemia. Some studies show that high concentrations of plasma triglycerides are related to hyperuricemia [ 58 , 62 - 64 ].
There are some explanations for such relation, and one of them is that during triglycerides TG synthesis there would be a greater need for NADPH [ 62 ]. The synthesis of fatty acids in the liver is associated with the de novo synthesis of purine, thus accelerating UA production [ 65 ]. Chen et al. The likely mechanism is the relationship between decreased HDL-C and insulin resistance [ 66 ].
Confirming this hypothesis, our research group showed that when adjusted for the other MS components, the relation between UA and HDL-c is lost [ 67 ]. In the adipose tissue, there is adipokine production, including that of leptin. One possible explanation for the association between higher waist circumference and hyperuricemia were suggested by Bedir et al. Some authors report UA to be responsible for blood pressure increase, and others show arterial hypertension AH to be a risk factor for hiperuricemia.
UA inhibits the bioavailability of nitric oxide, which is a vasodilator [ 70 ], and, on the other hand, AH would lead to vascular disease and increase renal vascular resistance. Both of these processes reduce renal flow, thus increasing urate resorption [ 71 ]. A recent study showed an inverse relation between muscle mass MM and UA in healthy individuals older than 40 years [ 72 ].
Chronic elevation of UA concentrations would be a causal factor for sarcopenia, especially through increased inflammation and oxidative stress [ 72 , 73 ]. The activation of the xanthine oxidase metabolic pathway, which increases UA production and the superoxide radical [ 74 ] could elevate the reactive oxygen species ROS and it could be the main mechanism for the reduction of MM.
Furthermore, UA exerts a pro-inflammatory effect, thus stimulating the production of interleukin-1, interleukin-6 the tumor necrosis factor which also can influence the muscle mass [ 75 ]. It is not known whether UA would be a causal factor or an antioxidant protective response against oxidative stress [ 76 ]. While chronic high UA concentrations are associated to increased risk for CAD, acute elevations seem to provide antioxidant protection [ 77 ]. Furthermore, the UA has a protective action in vitamins C and E [ 79 ] with the stabilizing activities in these vitamins [ 79 , 80 ] and the presence of ascorbic acid in plasma is required for the antioxidant effect of UA [ 80 ].
Also, it has a direct effect on the inhibition of free radicals such as peroxyl radical and peroxynitrite, protecting the cell membrane and DNA [ 81 , 82 ]. Most authors do not consider UA as a detrimental factor to the body health, because of its antioxidant function [ 8 , 83 ].
The antioxidant activity of UA also occurs in the brain [ 84 ], being a protector for several disease such as multiple sclerosis and neurodegenerative disease. Higher concentration of UA is associated with lower risk of development of Parksons disease and a favorable effect at the disease progression mainly [ 85 ].
Several factors are associated as cause and consequences of high UA concentration. Higher waist circumference and BMI are associated with higher insulin resistance and leptin production, and both reduce renal uric acid excretion, thus increasing its concentration. HDL-c concentration is negatively associated to insulin resistance, what can influence its negative correlation to uric acid.
Determinants of hyperuricemia. Additionally, obesity and muscle mass MM reduction are associated with low-intensity chronic inflammation, and uric acid levels can increase in order to protect the organism against the moderate oxidative stress resulting from this situation.
Low muscle mass sarcopenia is negatively associated with uric acid, However, it has not yet been clarified what the cause or effect is.
Probably, oxidative stress produced by excessive uric acid can influence muscle mass reduction. Furthermore, there is still no consensus if UA is a protective or a risk factor, however, it seems that the quantity and the duration of the concentration of the uric acid in the blood is essential for this answer.
Acute elevation seems to be a protective factor, whereas chronic elevation a risk factor. All authors read and approved. National Center for Biotechnology Information , U. Sections Basics Definition Causes When to see a doctor. Definition Causes When to see a doctor. Products and services. Thank you for Subscribing Our Housecall e-newsletter will keep you up-to-date on the latest health information. Please try again. Something went wrong on our side, please try again.
Show references Uric acid. Lab Tests Online. Accessed Oct. Questions and answers about gout. Kim SY, et al. Hyperuricemia and coronary heart disease: A systematic review and meta-analysis.
Ohno, I. Relationship between hyperuricemia and chronic kidney disease. Nucleosides, Nucleotides and Nucleic Acids. Kanbay M, et al. Uric acid in hypertension and renal disease: The chicken or the egg? Blood Purification.
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