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Uric acid displays lactam–lactim tautomerism. [4] Uric acid crystallizes in the lactam form, [5] with computational chemistry also indicating that tautomer to be the most stable. [6] Uric acid is a diprotic acid with pK a1 = 5.4 and pK a2 = 10.3. [7] At physiological pH, urate predominates in solution. [medical citation needed]
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]
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.
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]
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.
Crystals that can be found in normal urine include uric acid, monosodium urate, triple phosphate (ammonium magnesium phosphate), calcium oxalate, and calcium carbonate. [124] Crystals can also appear as poorly defined aggregates of granular material, termed amorphous urates or amorphous phosphates (urates form in acid urine while phosphates ...
In general, uricosuric drugs act on the proximal tubules in the kidneys, where they interfere with the absorption of uric acid from the kidney back into the blood.Several uricosurics are known to act in vitro by blocking the function of a protein encoded by the gene SLC22A12, also known as urate transporter 1 or URAT1.
This can occur because of diet, genetic predisposition, or underexcretion of urate, the salts of uric acid. [1] Underexcretion of uric acid by the kidney is the primary cause of hyperuricemia in about 90% of cases, while overproduction is the cause in less than 10%. [5]