Cam Kyle and Stephen Du Toit
About one third of body urate comes from the diet, two thirds from endogenous tissue catabolism. Under excretion of
urate by the kidneys is the cause of high serum levels in over 80% of adult patients. Insulin resistance (metabolic syndrome)
is associated with increased urate resorption and higher serum urate levels.
About 20% of males have a serum urate above 0.42 mmol/L, but this has been chosen as the upper end of the male range
because at that level urate becomes supersaturated in body fluids at 37�C, resulting in increased crystal deposition
in tissues. Above this level the 5�year risk of gout rises fifty-fold from about 0.1% below 0.42 mmol/L to 5% above 0.54
mmol/L. Above 0.60 mmol/L the 5�year prevalence of gout is about 30%.
An upper limit of 0.36 mmol/L is used for women because their levels before menopause average 0.06 mmol/L lower than
men. After menopause, levels in women approach those in men and the risk of gout increases, being similar to men over
Serum urate is the most important predisposing risk factor for gout, but is not used alone to make the diagnosis. Most
patients with high urate levels do not develop gout and, conversely, serum urate may be normal, especially during acute
attacks. Visual identification of crystals from joint fluid or tophi is the gold standard.
For patients with clinical gout on long-term treatment, a target urate level of 0.36 mmol/L has been recommended by
some international bodies. The long-term risk of gout recurrence is much lower when levels are maintained below this
threshold and it also favours the slow dissolution of chronic tophi, being well below the solubility constant of urate.
D-News, Diagnostic Medlab, August 2007 Available from: