Abstract
An experimental model for sustained hyperuricemia, uricosuria and associated nephropathy was produced by feeding rats a potent uricase inhibitor — sodium oxonate, together with dietary supplements of uric acid (1,2). In both human gouty nephropathy and in this experimental hyperuricemic nephropathy in rats, deposition of crystalline materials within the renal tubules and parenchyma have been observed (3). The deposition of urate crystals in the kidney could account for many of the inflammatory features of human gouty nephropathy, but the absence of a satisfactory experimental model has precluded detailed study of this possible relationship.
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Johnson, W.J., Stavric, B., Chartrand, A.: Uricase inhibition in the rat by S-triazines. An animal model for hyperuricemia and hyperuricosuria. Proc. Soc. Exp. Biol. Med. 131: 8, 1969.
Waisman, J., Bluestone, R., Klinenberg, J.: A prelminary report of nephropathy in hyperuricemic rats. Lab. Invest. 30: 716–722, 1974.
Bluestone, R., Brady, S., Waisman, J., and Klinenberg, J.R.: Experimental hyperuricemic nephropathy: A model for human urate deposition disease. Arth. Rheum. 18: 823–834, 1975.
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© 1977 Plenum Press, New York
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Klinenberg, J.R., Bluestone, R., Waisman, J. (1977). Suppression of Experimental Urate Nephropathy by Salicylate. In: Müller, M.M., Kaiser, E., Seegmiller, J.E. (eds) Purine Metabolism in Man—II. Advances in Experimental Medicine and Biology, vol 76B. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-3285-5_25
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DOI: https://doi.org/10.1007/978-1-4684-3285-5_25
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