PEDIATRICS Vol. 26 No. 6 December 1960, pp. 939-949
This Article
Right arrow Full Text (PDF)
Right arrow P3Rs: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when P3Rs are posted
Right arrow Alert me if a correction is posted
Services
Right arrow E-mail this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My File Cabinet
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kerpel-Fronius, E.
Right arrow Articles by Dobák, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kerpel-Fronius, E.
Right arrow Articles by Dobák, E.

INFLUENCES OF DEPLETION OF POTASSIUM, OF SODIUM, OR OF WATER ON FUNCTION AND STRUCTURE OF THE KIDNEY

E. Kerpel-Fronius M.D.1, G. Romhányi M.D.1, B. Gáti M.D.1, and E. Dobák M.D.1

1 Departments of Pediatrics and Pathology, University of Pécs, Hungary

Sublethal potassium losses were produced in rabbits by the repeated administration of theobromine. In experimental periods of 1 week, no significant decrease in the maximal concentrating ability of the kidneys, in creatinine urine:plasma (U:P) ratio and in creafinine clearance were observed, neither were histologic alterations evident.

See table in the PDF file

Prolongation of potassium deficiency (after theobromine-induced depletion) to 2-3 weeks by feeding a diet poor in potassium, reduced rabbits' ability to produce maximally concentrated urine, moderately decreased the creatinine clearance and induced damage in the renal collecting ducts and, subsequently, a striking dilatation of distal tubules. Presence or absence of metabolic alkalosis had no effect on renal alterations in potassium-depleted animals. Relations of structural (renal and myocardial) and functional alterations are discussed.

Sodium depletion reduced glomerular filtration rate (GFR) and concentrating ability much more than experimental potassium depletion. The defect in the concentrating mechanism is refractory to vasopressin both in sodium and in potassium depletion. Histologic changes accompanying sodium depletion consist in hydropic degeneration of the proximal convoluted tubules.