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The elevation of uric acid in blood is mainly due to an increase in its intake or a defect in its secretion. The mechanisms of renal damage go beyond the deposition of crystals at the tubular level; in this sense, renal damage also contributes to the production of chemotactic cytokines, cell proliferation, and inflammation, with the development of afferent arteriolopathy, glomerular hypertrophy and tubulointersticial fibrosis.
Nevertheless, whether or not hyperuricemia plays a causal role or simply is a marker arising in the course of each related disorder remains unresolved. Although a strong relationship between hyperuricemia and metabolic syndrome has been established through animal and epidemiological studies, the potential pathophysiological mechanisms by which uric acid contributes to this disease state are just beginning to be explained and clarified.
Measure ad performance. Select basic ads. Create a personalised ads profile. Select personalised ads. Apply market research to generate audience insights. Measure content performance. Develop and improve products. List of Partners vendors. When we urinate, our bodies eliminate liquid waste consisting of water and salt as well as the chemicals urea and uric acid. Most uric acid is produced naturally in the body; the rest is converted from substances in certain foods, called purines.
If uric acid levels are too high, they can cause a condition known as hyperuricemia, a risk factor for both gout and kidney disease. Most uric acid dissolves in the blood, then travels to the kidneys to be excreted in urine.
Normally, women maintain a stable serum urate level between 1. A blood test is one way to check your uric acid level; it can also be checked using a urine sample. Ideally, your serum uric acid level should be 6. Aging and being male put you at a higher risk of developing hyperuricemia. In studies from the U. While hyperuricemia itself is not a disease—and in some cases causes no symptoms or problems—a prolonged state of this condition may lead to the development of uric acid crystals, which can be problematic.
The two most common conditions that can result from high uric acid levels are gout and kidney disease. With gout, uric acid crystals build up in the joints, promoting inflammation and the breakdown of joint cartilage.
Symptoms include pain, swelling, redness, stiffness, deformity, inflammation, and limited range of motion. Uric acid crystals can also be deposited in the kidneys, causing kidney stones to form. These stones can be very painful and, if left untreated, can block the urinary tract and cause infections. Kidney stones can also cause urinary tract infections UTIs because they harbor bacteria. Over time, kidney stones and other forms of kidney damage can lead to chronic kidney disease , which makes it more difficult to get rid of uric acid.
Untreated kidney disease can ultimately lead to kidney failure or loss of kidney function. If you're not experiencing symptoms, you don't necessarily require treatment for hyperuricemia. When symptoms are present, a diet low in some non-plant-based purines may help regulate uric acid levels.
It's also important to drink plenty of water a day to help the kidneys flush out uric acid. Some studies suggest that drinking coffee on a regular basis can help prevent the development of gout.
When dietary changes do not sufficiently control hyperuricemia, your healthcare provider may prescribe medications to keep uric acid levels under control. Urate-lowering therapies are the preferred medication choice for most patients with gout.
Options include:. It is important to know your uric acid level, just as it is important to know your cholesterol or blood glucose levels. Mutations of its gene SLC2A9 are associated with aberrations of uric acid disposal.
Familial hyperuricemia due to uromodulin deficiency precedes but does not cause kidney failure. Nevertheless, both allopurinol and febuxostat treatment has sustained the hypothesis that hyperuricemia itself can have an adverse impact on kidney function.
Abstract Purpose of review: a To examine the latest information about renal tubular handling of uric acid, its genetic background and contribution to the causation of hyperuricemia.
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