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Uric acid is a normal waste product made by the body, but in some people, it can accumulate at higher levels and lead to gout. Gout can be divided into four stages: Hyperuricemia.
Treatment is focused on preventing deposition of uric acid within the urinary system by increasing urine volume with potent diuretics such as furosemide. Raising the urinary pH to a level higher than 7 (alkalinization) is often difficult to attain, although sodium bicarbonate and/or acetazolamide are sometimes used in an attempt to increase ...
Unless high blood levels of uric acid are determined in a clinical laboratory, hyperuricemia may not cause noticeable symptoms in most people. [5] Development of gout – which is a painful, short-term disorder – is the most common consequence of hyperuricemia, which causes deposition of uric acid crystals usually in joints of the extremities, but may also induce formation of kidney stones ...
Hyperuricosuria is a medical term referring to the presence of excessive amounts of uric acid in the urine. For men this is at a rate greater than 800 mg/day, and for women, 750 mg/day. [ 1 ] Notable direct causes of hyperuricosuria are dissolution of uric acid crystals in the kidneys or urinary bladder , and hyperuricemia .
In general, this effect is achieved by action on the proximal tubule of the kidney. Drugs that reduce blood uric acid are not all uricosurics; blood uric acid can be reduced by other mechanisms (see other Antigout Medications). Uricosurics are often used in the treatment of gout, a disease in which uric acid crystals form deposits in the joints.
Options for acute treatment include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and glucocorticoids. [20] While glucocorticoids and NSAIDs work equally well, glucocorticoids may be safer. [90] Options for prevention include allopurinol, febuxostat, and probenecid. Lowering uric acid levels can cure the disease. [5]
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