This Article  • References  • Full text PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citing articles on HighWire  • Citing articles on Web of Science (59)  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

Burton D. Cohen, MD

Arch Intern Med. 1970;126(5):846-850.

Abstract
Guanidinosuccinic acid (GSA), a nitrogenous metabolite isolated in excess from serum and urine, in uremia is a prime candidate for the role of a uremic toxin. It is excreted in small quantities by normal individuals at a relatively constant rate which increases after high protein intake. Twenty-four hour urinary excretion increases in animals following instillation of materials from which arginine is synthesized, is unchanged following those which are end products of arginine breakdown and is depressed in those conditions in humans which involve congenital absence of arginine synthetic enzymes. Guanidinoacetic acid, which suppresses arginine breakdown by a mechanism involving enzyme retroinhibition, is poorly excreted by the failing kidney and is, consequently, increased in uremic plasma. This is proposed as a mechanism for the genesis of GSA and suggests a method of detoxification.

Author Affiliations
Bronx, NY

From the Department of Medicine, the Bronx-Lebanon Hospital Center, Bronx, NY.

Footnotes
Received for publication July 8, 1970; accepted July 16.

Read before the session entitled "Protein Metabolism" (Carmelo Giordano, MD, chairman) of the Symposium on Uremic Toxins sponsored by the National Institute of Arthritis and Metabolic Diseases, Monterey, Calif, March 19, 1970.

Reprint requests to 1276 Fulton Ave, Bronx, NY 10456 (Dr. Cohen).

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

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Methylguanidine in Uremia
Giovannetti et al.
Arch Intern Med 1973;131:709-713.
ABSTRACT