Abstract
Recent theories on the physiopathology of Calcium Oxalate (Ca. Ox) nephrolithiasis proposed the supersaturation of urine for Ca. Ox as the main mechanism of stone formation. (1,2). It is obvious however that even in normals, urine might be saturated with Ca. Ox (3). An additionnai mechanism is then needed. The role of Uric Acid (U.A) or Urate has been suspected for several years. Three theories are currently under investigation:
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Heterogeneous nucleation with occurence of epitaxial growth of Ca. Ox on a nucleus made of a crystal of Monosodium (Na.U) or Ammonium Urate (NH4.U) (4);
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Excessive aggregation of Ca. Ox crystals due to a decrease in the normal inhibitory activity, this decrease being related to an increased urinary (total or colloidal) Na. U concentration (5).
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Facilitation of Ca. Ox precipitation due to a decreased formation product for Ca. Ox, depending on an increased U.A. urinary elimination (6).
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References
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© 1980 Plenum Press, New York
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Labeeuw, M., Gerbaulet, C., Pozet, N., Zech, P., Traeger, J. (1980). Urinary Urate and Uric Acid Relative Saturation in Normouricuric Calcium Oxalate Stone Formers with Normal Urinary Calcium Oxalate Saturation. In: Rapado, A., Watts, R.W.E., De Bruyn, C.H.M.M. (eds) Purine Metabolism in Man-III. Advances in Experimental Medicine and Biology, vol 122A. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-9140-5_14
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DOI: https://doi.org/10.1007/978-1-4615-9140-5_14
Publisher Name: Springer, Boston, MA
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