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Hyperuricaemia or hyperuricemia is an abnormally high level of uric acid in the blood. In the pH conditions of body fluid, uric acid exists largely as urate, the ion form. [1][2] Serum uric acid concentrations greater than 6 mg/dL for females, 7 mg/dL for males, and 5.5 mg/dL for youth (under 18 years old) are defined as hyperuricemia. [3]
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]
Hypouricemia. Hypouricemia or hypouricaemia is a level of uric acid in blood serum that is below normal. In humans, the normal range of this blood component has a lower threshold set variously in the range of 2 mg/dL to 4 mg/dL, while the upper threshold is 530 μmol/L (6 mg/dL) for women and 619 μmol/L (7 mg/dL) for men. [1]
Amino acid 2.7-5.5 × 10 −5: 2.4 ... varies with age ... Uric acid: child 2.0-6.7 × 10 ...
The HGPRT deficiency causes a build-up of uric acid in all body fluids. The combination of increased synthesis and decreased utilization of purines leads to high levels of uric acid production. This results in both high levels of uric acid in the blood and urine, associated with severe gout and kidney problems.
Gout is due to persistently elevated levels of uric acid (urate) in the blood (hyperuricemia). [4] [7] This occurs from a combination of diet, other health problems, and genetic factors. [3] [4] At high levels, uric acid crystallizes and the crystals deposit in joints, tendons, and surrounding tissues, resulting in an attack of gout. [3]
Acid–base and blood gases are among the few blood constituents that exhibit substantial difference between arterial and venous values. [6] Still, pH, bicarbonate and base excess show a high level of inter-method reliability between arterial and venous tests, so arterial and venous values are roughly equivalent for these.
Pathophysiology. Acute uric acid nephropathy is caused by deposition of uric acid crystals within the kidney interstitium and tubules, leading to partial or complete obstruction of collecting ducts, renal pelvis, or ureter. This obstruction is usually bilateral, and patients follow the clinical course of acute kidney failure .
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