Abstract
A group of patients forming calcium oxalate stones are hyperuricosuric and it is thought that their excessive urate excretion contributes to calcium-stones formation1. The pathomechanisms invoked are dietary purine excess and endogenous uric acid overproduction, being defective tubular reabsorption of urate “unattractive” because uricemia was found to be normal in patients with recurrent calcium nephrolithiasis (RCN) and hyperuricosuria. Current studies were undertaken to define the incidence, role of diet, abnormalities of the renal handling of urate, and associated metabolic disturbances in patients with RCN and hyperuricosuria.
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References
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© 1984 Plenum Press, New York
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Mateos, F., Puig, J.G., Martínez, E.M., Gaspar, G., Herrero, E., Piñeiro, J.A.M. (1984). Evidence of Abnormal Renal Handling of Uric Acid in Patients with Nephrolithiasis and Hyperuricosuria. In: De Bruyn, C.H.M.M., Simmonds, H.A., Müller, M.M. (eds) Purine Metabolism in Man-IV. Advances in Experimental Medicine and Biology, vol 165. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-4553-4_38
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DOI: https://doi.org/10.1007/978-1-4684-4553-4_38
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4684-4555-8
Online ISBN: 978-1-4684-4553-4
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