In the pH conditions of body fluid, uric acid exists largely as urate, the ion form.

Unless high blood levels of uric acid are determined in a clinical laboratory, hyperuricemia may not cause noticeable symptoms in most people.

[5] Gout symptoms are typically inflammation, swelling and redness of a joint, such as a toe or knee, accompanied by intense pain.

[12] In these metabolic myopathies, myogenic hyperuricemia is exercise-induced; inosine, hypoxanthine and uric acid increase in plasma after exercise and decrease over hours with rest.

AMP → IMP → Inosine → Hypoxanthine → Xanthine → Uric Acid[12] Hyperuricemia experienced as gout is a common complication of solid organ transplant.

[13] Apart from normal variation (with a genetic component), tumor lysis syndrome produces extreme levels of uric acid, mainly leading to kidney failure.

[19][20] Causes of hyperuricemia that are of mixed type have a dual action, both increasing production and decreasing excretion of uric acid.

[citation needed] Pseudohypoxia (disrupted NADH/NAD+ ratio), caused by diabetic hyperglycemia and excessive alcohol consumption, results in hyperuricemia.

The lactic acidosis inhibits uric acid secretion by the kidney, while the energy shortage from inhibited oxidative phosphorylation leads to increased production of uric acid due to increased turnover of adenosine nucleotides by the myokinase reaction and purine nucleotide cycle.

[21] High intake of alcohol (ethanol), a significant cause of hyperuricemia, has a dual action that is compounded by multiple mechanisms.

[22][23][24] In a large study in the United States, consumption of four or more sugar-sweetened soft drinks per day gave an odds ratio of 1.82 for hyperuricemia.

[27] The effect of fructose in reducing excretion of uric acid is increased in people with a hereditary (genetic) predisposition toward hyperuricemia and/or gout.

[29] Radioisotope studies suggest about 1/3 of uric acid is removed in healthy people in their gut with this being roughly 2/3 in those with kidney disease.

In people receiving hemodialysis, sevelamer can significantly reduce serum uric acid,[32][33] apparently by adsorbing urate in the gut.

If the person has chronic gout or known tophi, then large quantities of uric acid crystals may have accumulated in joints and other tissues, and aggressive and/or long duration use of medications may be needed.

[medical citation needed] Non-medication treatments for hyperuricemia include a low purine diet (see Gout) and a variety of dietary supplements.