URIC-ACID NEPHROLITHIASIS

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).