Abstract
Reduction in the renal mass is followed by a compensatory hypertrophy of the remaining kidney (1, 2). The search for the mechanism which triggers renal compensatory hypertrophy (RCH) has been the object of numerous investigations (1, 2). Despite intense efforts, the exact nature of the signal or signals which is/are implicated in the renal compensatory response have not yet been identified. Nevertheless, there is convincing evidence that RCH is triggered by an organ-specific humoral substance which is present in the plasma but may originate from the kidney itself (2, 6). The rate of compensatory growth has been shown to be influenced by various factors such as age (8), protein intake (9), and several hormones including growth hormone (10, 11), testosterone (12), thyroid hormone (13) and adrenal steroids (14). All these factors influence not only the “compensatory” growth but also the normal or “obligatory” growth of the kidney. Therefore, these factors appear to be rather unspecific since evidence has been obtained that RCH after unilateral nephrectomy is a growth phenomenon different from normal growth (15). An important feature which distinguishes the two phenomena is the fact that RCH is reversible, whereas normal growth is irreversible (15).
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References
Malt, R.A.: Compensatory growth of the kidney. N. Engl. J. Med. 280: 1446–1459 (1969).
Hayslett, J.P.: Functional adaptation to reduction in renal mass. Physiol. Rev. 59: 137–164 (1979)
Preuss, H.G., Terryl, E.F. and Keller, A.I.: Reno-tropic factor(s) in plasma from uninephrectomized rats. Nephron 7: 459–470 (1970).
Dicker, S.E. and Morris, C.A.: Presence of a renotropic factor in plasma of unilaterally nephrectomized rats. J. Physiol. 299: 13–27 (1980).
Hammond, G.L., Wieben, E. and Marker, C.C.: Molecular signals for initiating protein synthesis in organ hypertrophy. Proc. Natl. Acad. Sci USA 76: 24552459 (1979).
Dicker, S.E. and Morris, C.A.: Origin of the humoral factor responsible for compensatory renal hypertrophy. J. Physiol. 30: 1–5 (1980).
Galla, S.H., Klein-Robbenhaar, T. and Hayslett, J.P.: Influence of age on the compensatory response in growth and function to unilateral nephrectomy. Yale J. Biol. Med. 47: 218–226 (1974).
Ashinberg, L.C., Koskimies, O., Bernstein, J., Nash, M., Edelmann, C.M. and Spitzer, A.: The influence of age on the response to renal parenchymal loss. Yale J. Biol. Med. 51: 341–345 (1978).
Konishi, F.: Renal hyperplasia in young and old rats fed a high protein diet following unilateral nephrectomy. J. Gerontol. 17: 151–153 (1962).
Block, M.A., Wakim, K.G. and Mann, F.C.: Appraisal of certain factors influencing compensatory renal hypertrophy. Am. J. Physiol. 172: 60–66 (1953).
Astarabadim, T.: The effect of growth and lactogenic hormones on renal compensatory hypertrophy in hypophysectomized rats. Q. J. Exp. Physiol. 48: 85–91 (1963).
Schlondorff, D., Trizna, W., De Rosis, E. and Korth-Shutz, S.: Effect of testosterone on compensatory renal hypertrophy in the rat. Endocrinology 101: 1670–1675 (1977).
Reiter, R.J. In: The Endocrines and Compensatory Renal Enlargement in Compensatory Renal Hypertrophy. (W.W. Nowinski, ed.) New York, pp 183–204 (1969).
Goss, R.J.: Renal and adrenal relationships in compensatory hyperplasia. Proc.Soc.Exp.Biol.Med. 118: 342–346 (1965).
Silber, S. and Malvin, R.L.: Compensatory and obligatory renal growth in rats. Am.J.Physiol. 226: 114–117 (1974).
Whitfield, J.F., Boynton, J.P., MacManus, J.P., Sikorska, M. and Tsareg, B.K.: The regulation of cell proliferation by calcium and cyclic AMP. Mol. Cell. Biochem. 27: 155–179 (1979).
Whitfield, J.F., MacManus, J.P., Youdale, T. and Franks, D.J.: The roles of calcium and cyclic AMP in the stimulatory action of parathyroid hormone on thymic lymphocyte proliferation. J. Cell Physiol. 78: 355–368 (1971).
Rixon, R.H. and Whitfield, J.F.: Hypoplasia of the bone marrow in rats following removal of the parathyroid glands. J. Cell Physiol. 79: 348–352 (1972).
Rixon, R.H. and Whitfield, J.F.: Parathyroid hormone: A possible initiator of liver regeneration. Proc. Soc. Exp. Biol. Med. 141: 93–96 (1972).
Rixon, R.H. and Whitfield, J.F.: The control of liver regeneration by parathyroid hormone and calcium. J. Cell Physiol. 87: 147–155 (1976).
Rixon, R.H., MacManus, J.P. and Whitfield, J.F.: The control of liver regeneration by calcitonin, parathyroid hormone and 1,25-Dihydroxycholecalciferol. Mol. Cell Endocr. 15: 79–89 (1979).
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© 1984 Plenum Press, New York
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Bonjour, J.P., Jobin, J., Caverzasio, J., Taylor, C. (1984). Influence of Calcium and Calcium Regulating Hormones on Renal Compensatory Growth. In: Massry, S.G., Maschio, G., Ritz, E. (eds) Phosphate and Mineral Metabolism. Advances in Experimental Medicine and Biology, vol 178. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-4808-5_54
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DOI: https://doi.org/10.1007/978-1-4684-4808-5_54
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