Despite knowledge of uric acid that was identified at least 2 centuries ago, our understanding of hyperuricemia is not complete or sometimes clear. For years, hyperuricemia was thought to be the same as gout, but uric acid has now been recognized as a marker for a number of health complications such as metabolic and blood circulation abnormalities.
Uric acid, an end product of purine metabolism in humans, is poorly soluble or more difficult to dissolve. About two thirds of uric acid are produced internally, while the remaining third is obtained through dietary purines. In comparison to animals, humans have higher levels of uric acid, mostly due to a deficiency of involved enzymes and a comparatively lower rate of excretion of uric acid.
The kidneys are responsible for about 70% of daily uric acid excretion and the remaining 30% is filtered out by the intestines. In situations where the kidneys fail to keep up with this daily excretion, the intestinal elimination system will increase its load to compensate for the decreased amount of work by the kidneys. Uric acid blood levels are the tipping scale between the breakdown of purines and uric acid excretion rate. While it is believed that this balance can cause hyperuricemia, most clinical cases point to defective elimination as the primary cause for most cases of hyperuricemia.
Normal uric acid blood levels varies between genders, 2.4 - 6.0 mg/dL for women and 3.4 - 7.0 mg/dL for men. The upper limit for lies at 7.0 mg/dL where any higher puts you at risk for developing hyperuricemia. The cause of hyperuricemia is divided into three categories: uric acid underexcretion, uric acid overproduction or combined causes.
Underexcretion makes up most cases of hyperuricemia. Urate (a salt of uric acid) is filtered by the kidneys and undergoes a process that ends in the urate leaving the body through the urine. One misstep in this process can result in renal insufficiency and subsequently a poor rate of uric acid excretion. Underexcretion or poor kidney function can be caused by the following:
Overproduction occurs in a minority of patients who have hyperuricemia. Hyperuricemia induced by overproduction may be caused by external factors (high purine diet) or internal factors (increased purine breakdown). Overproduction of uric acid can be caused by the following:
A combination of overproduction and underexcretion can provide to be a problematic cause of hyperuricemia. The combination of both mechanisms can put patients at greater risks of developing complications. Combination causes can be a result of the following:
While specific life factors can contribute to hyperuricemia, studies have found that certain individuals or groups of people are more at risk to develop this condition. These factors include:
Gender
Hyperuricemia and its common successor gout are found to be more common in men than women. About 5% of gout patients are female, but the number tends to increase in women who experience menopause.
Age
Uric acid levels are typically lower in children than in adults. The likelihood to develop hyperuricemia increases with age with men ranging between 20 - 60 and women ranging between 40 and older. Individuals over 60+ are more likely to develop hyperuricemia and gout.
Race
Hyperuricemia caused by underexcretion is prevalent in races of the Pacific. Additionally, African Americans develop hyperuricemia more commonly than white Americans.
Health Conditions
Preexisting health conditions such as obesity, hypertension, diabetes and kidney problems have been linked to the development of hyperuricemia.
Hyperuricemia typically does not cause any physical symptoms, however if you incur any triggers or introduce factors that can cause other complications, you can expect or look out for the following:
Since hyperuricemia has a tendency to not develop any symptoms, it is best to consult with your doctor if you are concerned about your risk of developing hyperuricemia.
Hyperuricemia consists of two stages, asymptomatic and symptomatic.
Asymptomatic hyperuricemia
Most patients during this stage never develop gout or stones. Instead they are monitored and expected to make necessary changes to lower uric acid levels. Depending on the present urate levels, doctors will recommend lifestyle changes or prescribe medication to help lower uric acid levels. Asymptomatic hyperuricemia does not cause any symptoms and can for the most part go unrecognized unless a blood test is performed.
Symptomatic hyperuricemia
Patients who have hyperuricemia have developed physical symptoms or disorders such as gout, uric acid stones or uric acid nephropathy. Symptomatic hyperuricemia can also lead to other health complications that include:
Testing for hyperuricemia can be performed by your doctor. The following examinations can be conducted to determine your uric acid level and help to determine the next steps for treatment and prevention of other health risks.
Lab Testing and Examinations:
Imaging Studies
Medications prescribed to patients with hyperuricemia are designed to help reduce and prevent the risk of developing complications. Typically, medications will address high uric acid levels and those prescribed will help counter overproduction of the waste product. Other medications can be prescribed based on any other complications a patient experiences such as gout or kidney related disorders.
Function: designed to prevent gout attacks and used to treat hyperuricemia by preventing the activity of the enzyme xanthine oxidase.
Medications: allopurinol, febuxostat
Function: inhibit the reabsorption of uric acid and promotes the excretion of uric acid while simultaneously lowering urate levels.
Medications: probenecid
Function: facilitates the conversion of urate to a more soluble product, such as allantoin.
Medications: pegloticase, rasburicase
Function: used to raise the pH in urine.
Medications: potassium citrate
Function: influence a variety of metabolic effects and modify the body’s immune response.
Medications: prednisone, dexamethasone
Function: decrease the solubility of uric acid, combined with an adequate hydration intake increases the benefits of this medication.
Medications: acetazolamide
Function: prescribed for patients suffering with gout to treat active attacks and prevent recurrence.
Medications: colchicine
Function: management of pain and inflammation caused by gout.
Medications: indomethacin
Hyperuricemia is an easily treatable disorder that requires some patient education and understanding on the condition. Patients who have asymptomatic hyperuricemia are urged to make lifestyle changes that can help maintain uric acid levels. Those with symptomatic hyperuricemia are encouraged to perform regular follow-up evaluations to determine current urate levels and to monitor progress. Hyperuricemia is preventable by following making the following lifestyle changes:
Reducing purines in the diet can have a significant impact on uric acid levels and is a huge part of management and prevention. Certain foods contain more purines than others and it’s important to become familiar with them.
Patients with a history of drinking fructose sweetened drinks and having a high sugar consumption have a tendency to have raised uric acid levels. By moderating your sugar intake you can prevent the contribution to a uric acid level imbalance.
Alcohol consumption can lead to the overproduction and underexcretion of uric acid. By avoiding and significantly lessen your chances or developing hyperuricemia.
Fat tissue tends to hold urate and when the tissue is broken down, it can release the accumulated uric acid causing a rise in blood levels. Additionally, obesity and being overweight can put a strain on your kidneys, affecting their function and contributing to underexcretion.
Gout is a painful inflammatory arthritis disease caused by deposits of uric acid crystals in the joints and articular tissues. In most cases, gout is caused by certain lifestyle factors such as obesity, usage of medications and poor diet, all of which can lead to a high level of uric acid in the body. High levels of uric acid lead to the development of the condition known as hyperuricemia, and while only 20% of people with hyperuricemia ever develop gout, in most cases the two are often causation factors of one another.
Hyperuricemia is an indicator for poor management of uric acid levels in the body. Whether it be the overproduction or underexcretion of uric acid - or a combination of the two, there is a significant disconnect in the maintenance of uric acid in the blood. 20% of hyperuricemia patients have been observed to develop gout if their uric acid levels are not managed, implying that there is a direct connection between hyperuricemia and gout.
It is important to note however, that most cases of hyperuricemia do not lead to gout, but instead can lead to other health complications related to kidney, liver and heart function. Additionally, unlike gout, hyperuricemia does not cause any significant physical symptoms. Hyperuricemia becomes symptomatic when you develop other complications such as gout, renal failure or liver disease.
When it comes to asymptomatic hyperuricemia in most cases treatment isn’t necessary. Instead it is encouraged that efforts be made to lower urate levels, this includes making changes to diet or lifestyle. A treatment plan is administered for symptomatic hyperuricemia and when complications such as gout, kidney disease or renal insufficiency develop. Treatment for symptomatic hyperuricemia will vary based on the specific complication and other conditions that need to be addressed.
Dietary modifications are the most critical step in lowering urate levels. Adopting eating habits that correlate with the decrease uric acid production is highly recommended as compared to committing to lifelong therapy for an asymptomatic condition.
When it comes to urate lowering dietary restrictions, key things to remember is reducing or avoiding purine-rich foods such as organ or red meats, shellfish and avoiding excessive alcohol consumption, especially beer.
Foods to Avoid
Foods to Eat
Putting it all together: To get ideas or learn how to put together a purine-reduced eating plan, visit our recipe section for inspiration or check out our Anti-Gout nutrition plan.
Complementary Supplements
Supplements are a great addition to your therapy and can help provide you with vitamins and minerals that you might not be getting enough of from your diet. In addition, some supplements have been recognized to act as natural urate lowering substances and can be helpful in managing your uric acid levels. Supplements to add to your diet include:
The following drug agents have been recognized to cause overproduction or underexcretion of uric acid:
Hyperuricemia should be addressed by making an effort towards dietary and lifestyle changes. These changes include adopting a diet that is reduced in purines, limits alcohol consumption and sugar intake and also promotes weight loss and daily exercise.
There has been effective homeopathic treatments recognized for hyperuricemia.
According to a study, hyperuricemia has been linked to feelings of dizziness.
Rifampin has been associated with liver dysfunction and may contribute to elevated uric acid levels.
Urate acid deposits can cause some itching.
Symptomatic hyperuricemia can lead to renal failure if left untreated.
Alcohol increases the production of uric acid and also produces competing compounds that lead to the decrease of uric acid excretion by the kidneys.
Diuretics cause the body to have low fluid retention, making it difficult for uric acid to be completely deposited from the body.
Low-dose aspirin can influence renal function and how the kidneys handle uric acid leading to underexcretion of the waste product and thus hyperuricemia.
Ethambutol can influence renal function and how the kidneys handle uric acid leading to underexcretion of the waste product and thus hyperuricemia.
Furosemide can influence renal function and how the kidneys handle uric acid leading to underexcretion of the waste product and thus hyperuricemia.
HCTZ is a diuretic that enables the reabsorption of urate into the body, leading to poor excretion of uric acid.
The mechanics of how hyperuricemia causes hypertension is not yet understood, however based on multiple clinical research, hyperuricemia has been recognized as a causation factor for hypertension.
Leukemia can influence renal function and efficiency, contributing to the underexcretion of uric acid.
Niacin’s agents are known to compete with uric acid for excretion by the kidneys, leading to underexcretion of uric acid.
Leptin, a gene production of obesity, has been found to interact with uric acid resulting in increasing levels and hyperuricemia.
Pyrazinamide inhibits the excretion of urate, leading to poor depositing of the waste product.
Thiazide’s agents are known to compete with uric acid for excretion by the kidneys, leading to underexcretion of uric acid.
Von gierek’s disease is a form of glucose-6-phosphatase deficiency that causes poor renal function and also influences the overproduction of waste products (including uric acid and lactic acid) that compete with uric acid for renal excretion. It is a combination causation factor of hyperuricemia.
Please ask your doctor.
Hyperuricemia and diabetes are often associated with one another as the two are a result of poor dietary and lifestyle choices.
Xanthine oxidase is the enzyme responsible for the formation of uric acid. It is activated when purines enter the body and proceeds to initiate the breakdown of the substance and produce the waste product, uric acid.
Untreated and prolonged hyperuricemia can cause heart disease and failure.
Untreated and prolonged hyperuricemia can become symptomatic and cause a series of complications, the most morbid including, kidney and liver disease or failure and heart disease or failure.
Symptomatic hyperuricemia can lead to the development of gout, kidney stones, kidney complications (such as disease and failure) and liver complications. These complications can all be very painful and drastically affect your quality of life.
Familial juvenile hyperuricemia is a dominantly inherited condition that is characterized by young-onset hyperuricemia, gout and renal disease.
Oatmeal is a cereal that is not significantly high in purines and can be consumed by anyone that has high uric acid levels. Unless you suffer from a specific purine metabolism disorder, there is no reason to avoid oatmeal. The key to consuming oatmeal is moderation.
Oliguria is a condition in which the production of urine is abnormally low. This can lead to underexcretion of uric acid and result in hyperuricemia.
Quercetin has been observed in vitro to act as a natural xanthine oxidase inhibitor and has been thought to help with lowering uric acid levels.
Uncontrolled and neglected hyperuricemia can become symptomatic and cause a series of complications, the most morbid including, kidney and liver disease or failure and heart disease or failure.
Asymptomatic hyperuricemia is a stage of hyperuricemia where uric acid levels in the blood are over 7.0 mg/dL, but the patient experiences no symptoms. During this stage, patients are recommended to make dietary and lifestyle changes to reduce uric acid concentration to lower levels.
Yes.
Hyperuricosuria is the prevalence of excessive amounts of uric acid in the urine, hyperuricemia is the presence of excessive uric acid in the blood.
Hyperuricemia can lead to the development of kidney complications such as kidney disease, kidney stones, renal dysfunction and kidney failure.
Dialysis may be a therapy option introduced for severe hyperuricemia and with other health conditions are furthering complications.
Preeclampsia and eclampsia, are two pregnancy complications that are associated with high levels of uric acid.
Edema can be a complication that develops as a result of untreated hyperuricemia.
Chronic fatigue can be associated with hyperuricemia.
Fatty liver has been recognized to significantly increase the risk of hyperuricemia.
Beta blockers are known to contribute to increased uric acid levels. The mechanism of this medication is not fully understood, but is a common factor among hyperuricemia patients.
Fructose intolerance results in the increased degradation of products that can be converted to uric acid and thus increase levels in the body leading to hyperuricemia.
Hyperuricemia can lead to the development of gout, a painful arthritis that affects the big toe joint, ankle and knees.
Chemotherapy agents can contribute to the overproduction of uric acid, resulting in hyperuricemia.
While hyperuricemia itself is not genetic, genetic disorders related to poor renal function and subsequently poor regulation of uric acid levels can contribute to hyperuricemia.
Bodybuilders who follow a high protein diet are typically consuming high purine foods that lead to elevated uric acid levels and the possible development of hyperuricemia.
Hyperuricemia is prevalent among men, aged 20 - 60 and is likely to develop following a high purine diet, excessive alcohol consumption and high sugar intake.
Rheumatoid arthritis is rarely found in hyperuricemia patients. About 10% of rheumatoid arthritis patients have high uric acid blood levels.
Yes, morbid complications include kidney, liver and heart failure.
Yes.
Ask your doctor.
Normal uric acid blood levels varies between genders, 2.4 - 6.0 mg/dL for women and 3.4 - 7.0 mg/dL for men. The upper limit for lies at 7.0 mg/dL where any higher puts you at risk for developing hyperuricemia.
Osteoarthritis can be mistaken for gout (an arthritis disease that can develop if hyperuricemia is left unaddressed) since the two diseases share characteristic of inflammation, pain and swelling.
Patients with psoriasis have been identified to have a greater prevalence of hyperuricemia. This connection however is not completely understood as further clinical research has not been conducted.
Skin rashes can develop if taking medications such as allopurinol to help with hyperuricemia.
Hyperuricemia can contribute to cardiovascular complications that can sometimes result in a stroke.
Please refer to our supplements page
Hyperuricemia is often associated with uremia due to its potential influence on renal function that can lead to uremia.
Vitamin B12 has been linked to the overproduction of uric acid and can lead to hyperuricemia and gout.
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