The potential importance of uric acid, monopotassium urate, monoammonium urate and monosodium urate in the pathogenesis of hyperuricosuric calcium oxalate nephrolithiasis was explored. Urinary pH in patients with this disorder was not found to be significantly different from that found in patients with absorptive hypercalciuria [5.91 ± (SD) 0.32 vs. 6.04 ± 0.33]. Uric acid was ineffective in inducing heterogeneous nucleation of Ca oxalate, in binding heparin, or in attenuating heparin-induced inhibition of Ca oxalate nucleation. Because of undersaturation, monopotassium urate is unlikely to form in urine. Moreover, it did not cause heterogeneous nucleation of Ca oxalate, bind heparin, or attenuate heparin action. Urine samples were often supersaturated with respect to monoammonium urate and monosodium urate. Although monoammonium urate failed to induce heterogeneous nucleation of Ca oxalate, it bound heparin and reduced the inhibitory effect of heparin on Ca oxalate nucleation. Monosodium urate, which was shown previously to cause heterogeneous nucleation of Ca oxalate and bind heparin, was more effective than monoammonium urate in binding heparin and attenuating glucosaminoglucan action. Thus, monosodium urate displayed the most prominent role in Ca oxalate crystallization among the four urate phases tested.
|Original language||English (US)|
|Number of pages||7|
|Journal||Mineral and Electrolyte Metabolism|
|State||Published - Jan 1 1980|
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism