Uric acid is the end-product of purine nucleotide metabolism in man. T
he renal handling of urate is a complicated process, resulting in a fr
actional clearance of 8.2 - 10.3%, The anhydrous form is thermodynamic
ally the most stable uric acid crystal. Uric acid is a weak acid that
ionizes with a Pka at pH 5.75. At the normal acidic region, uric acid
solubilty is strongly increased by urinary pH. The prevalence of uric
acid stones varies between countries, reflecting climatic, dietary, an
d ethnical differences, ranging from 2.1% (in Texas) to 37.7% (in Iran
). The risk for uric acid stone formation correlates with the degree o
f uric acid supersaturation in the urine, depending on uric acid conce
ntration and urinary pH. Hyperuricosuria is the major risk factor, the
most common cause being increased purine intake in the diet, Acquired
and hereditary diseases accompanied by hyperuricosuria and stone dise
ase include: gout, in strong correlation with the amount of uric acid
excreted, myelo- and lymphoproliferative disorders, multiple myeloma,
secondary polycythemia, pernicious anemia and hemolytic disorders, hem
oglobinopathies and thalassemia, the complete or partial deficiency of
HGPRT, superactivity of PRPP synthetase, and hereditary renal hypouri
cemia. A common denominator in patients with idiopathic and gouty ston
e formers is a low urinary pH. Uric acid nephrolithiasis is indicated
in the presence of a radiolucent stone, a persistent undue urine acidi
ty and uric acid crystals in fresh urine samples. A radiolucent stone
in combination with normal or acidic pH should raise the possibility o
f urate stones. Uric acid stones can be effectively treated and preven
ted by increasing the solubility of urinary uric acid. This is obtaine
d by increasing urine volume, by augmenting urinary pH and by decreasi
ng uric acid production (by decreasing dietary purine intake and by ph
armacological inhibition of uric acid formation by allopurinol).