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Influence of Calcium and Calcium Regulating Hormones on Renal Compensatory Growth

  • J. P. Bonjour
  • J. Jobin
  • J. Caverzasio
  • C. Taylor
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 178)

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).

Keywords

Parathyroid Hormone Liver Regeneration Renal Mass Compensatory Growth Unilateral Nephrectomy 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Press, New York 1984

Authors and Affiliations

  • J. P. Bonjour
    • 1
    • 2
  • J. Jobin
    • 1
    • 2
  • J. Caverzasio
    • 1
    • 2
  • C. Taylor
    • 1
    • 2
  1. 1.Department of PathophysiologyUniversity of BerneSwitzerland
  2. 2.Division of Pathophysiology, Department of MedicineUniversity of GenevaSwitzerland

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