This Article  • References  • Full text PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

Neil A. Kurtzman, MD; Veerasamy K. G. Pillay, MB

Arch Intern Med. 1973;131(6):901-904.

Abstract
Glucose reabsorption has been recently shown to be linked to that of sodium. When sodium reabsorption is enhanced, so is glucose reabsorption; when sodium reabsorption is depressed, so is that of glucose. Glucose reabsorption, like that of sodium, is also tied to the glomerular filtration rate (GFR), increasing when the GFR increases and falling when the GFR falls (glomerular tubular balance). Thus, no maximal rate of tubular reabsorption exists for glucose, at least in the classical sense. Those altered states of homeostasis accompanied by hyperglycemia and volume contraction (the major stimulus to increased renal reabsorption of sodium) will also be accompanied by increased glucose reabsorption that will both accentuate and perpetuate the hyperglycemia.

Author Affiliations
Chicago

From the University of Illinois, Abraham Lincoln School of Medicine, Chicago.

Footnotes
Received for publication Jan 15,1973; accepted Feb 6.

Reprint requests to University of Illinois, Abraham Lincoln School of Medicine, Chicago 60612 (Dr. Kurtzman).

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Angiotensin-Converting Enzyme Inhibitors and Glycosuria
Milavetz and Popovtzer
Arch Intern Med 1992;152:1081-1083.
ABSTRACT