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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.
Those with gout are at increased risk of hypertension, diabetes mellitus, metabolic syndrome, and kidney and cardiovascular disease and thus are at increased risk of death. [ 5 ] [ 104 ] It is unclear whether medications that lower urate affect cardiovascular disease risks. [ 105 ]
Left ventricular hypertrophy. Hypertensive heart disease is the result of structural and functional adaptations [18] leading to left ventricular hypertrophy, [19] [20] [21] diastolic dysfunction, [18] [20] CHF (Congestive Heart Failure), abnormalities of blood flow due to atherosclerotic coronary artery disease [18] and microvascular disease, [10] [19] and cardiac arrhythmias. [19]
Uric acid is a heterocyclic compound of carbon, nitrogen, oxygen, and hydrogen with the formula C 5 H 4 N 4 O 3. It forms ions and salts known as urates and acid urates, such as ammonium acid urate. Uric acid is a product of the metabolic breakdown of purine nucleotides, and it is a normal component of urine. [1]
By decreasing plasma uric acid levels, help dissolve these crystals, while limiting the formation of new ones. However, the increased uric acid levels in urine can contribute to kidney stones. Thus, use of these drugs is contraindicated in persons already with a high urine concentration of uric acid (hyperuricosuria). In borderline cases ...
Uric acid competes with lactic acid and other organic acids for renal excretion in the urine. In GSD I increased availability of G6P for the pentose phosphate pathway, increased rates of catabolism, and diminished urinary excretion due to high levels of lactic acid all combine to produce uric acid levels several times normal.
Once the diagnosis of hypertension has been made, further testing may be performed to find secondary hypertension, identify comorbidities such as diabetes, identify hypertension-caused organ damage such as chronic kidney disease or thickening of the heart muscle, and for cardiovascular disease risk stratification.