How Hyperuricemia Occurs
Hyperuricemia, or gout without any known precipitating cause, is a relatively recent discovery. Although differing definitions vary widely across the medical literature based on different criteria, hyperuricemia most often is associated with renal and cardiovascular diseases. But whether or not it acts as an independent condition or merely a bystander still is to be determined. Thus, the Ayurvedic treatment of hyperuricemia remains mostly at the preventive level, in order to avoid any further damage to the kidneys and to protect the rest of the body against any further attacks of gout.
It has been postulated that hyperuricemia may itself be the result of a defective gene or protein transfer, whereby some regulatory proteins were impaired within the kidneys. This theory was tested by carrying out genetic tests on mice, which resulted in the mutations of regulatory genes responsible for producing the purines. It was thus concluded that hyperuricemia was caused by a defect in the gene regulation mechanism, whereby the pathway was interrupted at the point where the purines arrived in the kidney. The drugs used in such a situation could therefore be useful in controlling and eventually stopping hyperuricemia and its resulting related symptoms.
The other proposed explanation for hyperuricemia derives from the fact that purine metabolism plays a major role in the pathophysiology of gout. Gout is a form of arthritis and the high uric acid levels, which characterize this disease have been associated with high purine diets. Therefore, it was reasoned that hyperuricemia might also be caused by high purine intake. It was accordingly found that patients with gout had high levels of uric acid in their urine, which were indicative of hyperuricemia.
The third proposed mechanism for hyperuricemia relates to the kidneys themselves. The kidneys are supposed to excrete vast quantities of uric acid in the urine, especially in situations where they are being worked upon by drug therapy, for example during the treatment of rheumatoid arthritis. In such a situation, the kidneys are supposed to abnormally regulate the production of uric acid, causing the high serum uric acid levels, which are the main symptoms of hyperuricemia. Drugs such as allopurinol and colchicine are used to treat hyperuricemia, along with a combination of surgery and kidney transplantation.
Another factor which might lead to hyperuricemia and its resultant joint pains is the influence of crystals in the joints. Since uric acid levels in the blood are determined largely by the mineral status of the body, it is suggested that the kidneys play an important role in their excretion. Accordingly, people suffering from the kidney failure complication ameliorate the hyperuricemia, by reducing the quantity of uric acid crystals, through their ability to filter out excess water from the blood, and by their ability to retain liquids in the joints. It has been found that the crystallized urate, which is normally excreted by the kidneys, accumulates in the joints, particularly the intervertebral discs. These discs can degenerate with age, causing painful intervertebral discogenicgia.
Diet plays an important role in dealing with hyperuricemia, since the reduction in dietary acid reduces the quantity of crystals in the urine. It is also believed that dietary changes can help in the prevention of the progression of this condition. A diet which is rich in fruits, vegetables and whole grains, rich in protein, minerals and low in fat, helps reduce the risk of developing hyperuricemia and its resulting complications. Thus, it is concluded that a proper diet can prevent the development of stones, especially kidney stones, and can reduce the severity of their effects.
More Gout Resources
- List of Vegetables Good for Gout
- Can Carrots Lower Uric Acid?
- Does Soft Drinks Like Coca Cola Increase Uric Acid?
- Foods to avoid Hyperuricemia
- How Diuretics Cause Hyperuricemia
- How Hyperuricemia Leads To Gout
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