A Placebo Controlled Double-Blind Study of Allopurinol in Severe Recurrent Idiopathic Renal Lithiasis. Preliminary Results
Recently the possible role of mild disorders of purine, uric acid and/or urate metabolism in renal stone formation has been emphasised1,2. When urine pH increases above 5.7, uric acid dissociates to urate which can then form sodium urate in the presence of sodium ions. When urinary pH approaches 6.0, the sodium urate/uric acid balance favours urate formation. Although the former is more soluble than the latter, sodium urate can precipitate if its urinary concentration increases sufficiently3,4. One hypothesis suggests that if the urine is metastable with respect to calcium oxalate and/or calcium phosphate, precipitation of these salts may be initiated through heterogeneous nucleation by sodium urate5. The second hypothesis is that a colloidal form of sodium urate binds certain crystal-inhibiting substances in urine, e.g. the glycosaminoglycans (GAGS), with a consequent decrease in the ability of urine to inhibit crystal growth and aggregation6. Previous clinical studies on calcium stone formers with disorders of uric acid metabolism have shown a marked reduction in stone formation with allopurinol. We therefore undertook a double-blind study in a group of patients with recurrent idiopathic calcium oxalate stones.
KeywordsUric Acid Stone Formation Calcium Oxalate Serum Urate Urinary Uric Acid
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- 6.W. G. Robertson, F. Knowles, and M. Peacock, in: “Urolithiasis Research”, H. Fleisch, W. G. Robertson, L. H. Smith, and W. Vahlensieck, eds., Plenum, New York (1976).Google Scholar