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Amendment history:
  • Errata (September 1968)

Research Article Free access | 10.1172/JCI105772

Functional correlates of compensatory renal hypertrophy

John P. Hayslett, Michael Kashgarian, and Franklin H. Epstein

Department of Internal Medicine, Yale University School of Medcine, New Haven, Connecticut 06500

Department of Pathology, Yale University School of Medcine, New Haven, Connecticut 06500

Find articles by Hayslett, J. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, Yale University School of Medcine, New Haven, Connecticut 06500

Department of Pathology, Yale University School of Medcine, New Haven, Connecticut 06500

Find articles by Kashgarian, M. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, Yale University School of Medcine, New Haven, Connecticut 06500

Department of Pathology, Yale University School of Medcine, New Haven, Connecticut 06500

Find articles by Epstein, F. in: JCI | PubMed | Google Scholar

Published April 1, 1968 - More info

Published in Volume 47, Issue 4 on April 1, 1968
J Clin Invest. 1968;47(4):774–782. https://doi.org/10.1172/JCI105772.
© 1968 The American Society for Clinical Investigation
Published April 1, 1968 - Version history
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Abstract

The functional correlates of compensatory renal hypertrophy were studied by micropuncture techniques in rats after the removal of one kidney. The glomerular filtration rate increased to roughly the same extent in the whole kidney and in individual surface nephrons, resulting in a greater amount of sodium delivered to the tubules for reabsorption. The fraction of the glomerular filtrate absorbed [determined from the tubular fluid-to-plasma ratio (TF/P) for inulin] remained unchanged in both proximal and distal portions of the nephron. The way in which the tubules adjusted to nephrectomy, however, differed in proximal and distal convolutions. After nephrectomy, the reabsorptive half-time, indicated by the rate of shrinkage of a droplet of saline in a tubule blocked with oil, was unchanged in the proximal tubule but significantly shortened in the distal convoluted tubule. Nevertheless, steady-state concentrations of sodium in an isolated raffinose droplet in the distal as well as the proximal tubule were the same in hypertrophied kidneys as in control animals. Possible reasons for this paradox are discussed.

Transit time through the proximal tubules was unchanged by compensatory hypertrophy, but transit time to the distal tubules was prolonged.

Changes in renal structure resulting from compensatory hypertrophy were also found to differ in the proximal and the distal protions of the nephron. Although tubular volume increased in both protions, the volume increase was twice as great in the proximal tubule as in the distal. In order, therefore, for net reabsorption to increase in the distal tubule, where the changes in tubular volume are not so marked, an increase in reabsorptive capacity per unit length of tubule is required. This increase is reflected in the shortening of reabsorptive half-time in the oil-blocked distal tubule that was actually observed.

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