Abstract
Excess dietary phosphate produces progressive increase in calcium content of the kidney and also leads to progressive deterioration of renal function1–3. The important variables responsible for determination of both the rate of deposition of calcium and loss of renal function are the quantity of dietary phosphate, the amount of functioning renal tissue and the level of parathyroid activity3,4. Given sufficient reduction in the size of the functioning renal mass, progressive deposition of calcium can be demonstrated in the kidney of animals maintained on a diet of normal phosphate content5. The histologic changes associated with these progressive calcium deposits provide convincing evidence of the structural damage produced, apparently resulting from cellular damage associated with calcium phosphate deposition 3,6.
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© 1982 Plenum Press, New York
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Walker, W.G., Gimenez, L., Tew, W.P., Hermann, J.A. (1982). Prevention of Phosphate Induced Progression of Experimental Uremia by 3-Phosphocitric Acid. In: Massry, S.G., Letteri, J.M., Ritz, E. (eds) Regulation of Phosphate and Mineral Metabolism. Advances in Experimental Medicine and Biology, vol 151. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-4259-5_21
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DOI: https://doi.org/10.1007/978-1-4684-4259-5_21
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