Mechanism of change in the excretion of sodium per nephron when renal mass is reduced

John P. Hayslett; Michael Kashgarian; Franklin H. Epstein

doi:10.1172/JCI106056

^{Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06525}

^{Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06525}

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^{Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06525}

^{Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06525}

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

^{Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06525}

^{Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06525}

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Published in Volume 48, Issue 6 on June 1, 1969
J Clin Invest. 1969;48(6):1002–1006. https://doi.org/10.1172/JCI106056.
© 1969 The American Society for Clinical Investigation

Published June 1, 1969 - Version history

As the population of nephrons is reduced, sodium excretion per nephron must increase if sodium balance is to be maintained. The mechanism of this adjustment was studied in rats in which 50% and approximately 85% of renal tissue was excised. Although glomerular filtration per remaining nephron rose after uninephrectomy, it did not rise further when more renal tissue was removed, even though sodium excretion per nephron mounted. Hyperfiltration does not, therefore, account for the stepwise increase in sodium excretion per nephron with progressive renal ablation. Proximal tubular absorption, estimated by reabsorption half-time, was unchanged by renal insufficiency, indicating that “third factor” did not produce the observed changes in sodium excretion per nephron. It seems likely that the earliest adjustments in sodium excretion in renal failure take place in the distal tubules of healthy nephrons, and that they are conditioned by changes in the osmotic load per nephron.

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