Abstract
Most patients with primary gout show a relative underexcretion of uric acid when compared to normal subjects (1–3). It has been suggested that an alteration in the tubular transport of uric acid could reflect a more extensive defect which might involve related compounds (4). Hypo-xanthine and xanthine are intermediates of the purine nucleotide degradation pathway. Disturbances of hypoxanthine and xanthine metabolism may provide important insights for better understanding the mechanism underlying primary gout.
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© 1989 Plenum Press, New York
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Puig, J.G., Mateos, F.A., Jiménez, M.L., Ramos, T., Capitán, M.C., Gil, A.A. (1989). Impaired Renal Excretion of Hypoxanthine and Xanthine in Primary Gout. In: Mikanagi, K., Nishioka, K., Kelley, W.N. (eds) Purine and Pyrimidine Metabolism in Man VI. Advances in Experimental Medicine and Biology, vol 253A. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5673-8_45
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DOI: https://doi.org/10.1007/978-1-4684-5673-8_45
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