Uric acid is the end-product of
purine nucleotide metabolism in man. The renal handling of
urate is a complicated process, resulting in a fractional clearance of 8.2-10.3%. The anhydrous form is thermodynamically 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 solubility is strongly increased by urinary pH. The prevalence of
uric acid stones varies between countries, reflecting climatic, dietary, and ethnical differences, ranging from 2.1% (in Texas) to 37.7% (in Iran). The risk for
uric acid stone formation correlates with the degree of
uric acid supersaturation in the urine, depending on
uric acid concentration 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 disease 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,
hemoglobinopathies and
thalassemia, the complete or partial deficiency of
HGPRT, superactivity of
PRPP synthetase, and hereditary
renal hypouricemia. A common denominator in patients with idiopathic and gouty stone formers is a low urinary pH.
Uric acid nephrolithiasis is indicated in the presence of a radiolucent stone, a persistent undue urine acidity and
uric acid crystals in fresh urine samples. A radiolucent stone in combination with normal or acidic pH should raise the possibility of
urate stones.(ABSTRACT TRUNCATED AT 250 WORDS)