PROLONGED HYPERALIMENTATION AS A POSSIBLE CAUSE OF RENAL TUBULAR DYSFUNCTION - EVALUATION OF 1,5-ANHYDRO-D-GLUCITOL RESORPTION AND N-ACETYLGLUCOSAMINIDASE EXCRETION IN HUMANS

Citation
T. Yamanouchi et al., PROLONGED HYPERALIMENTATION AS A POSSIBLE CAUSE OF RENAL TUBULAR DYSFUNCTION - EVALUATION OF 1,5-ANHYDRO-D-GLUCITOL RESORPTION AND N-ACETYLGLUCOSAMINIDASE EXCRETION IN HUMANS, Clinical science, 88(2), 1995, pp. 203-210
Citations number
27
Categorie Soggetti
Medicine, Research & Experimental
Journal title
ISSN journal
01435221
Volume
88
Issue
2
Year of publication
1995
Pages
203 - 210
Database
ISI
SICI code
0143-5221(1995)88:2<203:PHAAPC>2.0.ZU;2-G
Abstract
1. A major polyol found in the sera and other tissues of humans, 1,5-a nhydro-D-glucitol, is mainly ingested in the diet and is excreted in u rine, We compared the influence of the long-term administration of tot al parenteral nutrition free of 1,5-anhydro-D-glucitol with that of to tal enteral nutrition on the serum level of 1,5-anhydro-D-glucitol in 46 patients who could not take food by mouth. 2. The serum concentrati on of 1,5-anhydro-D-glucitol and its kinetics remained unchanged in th e group receiving total enteral nutrition (n = 21) over a period of 12 months, However, after 1 month on total parenteral nutrition (n = 25) , the serum level of 1,5-anhydro-D-glucitol decreased, falling to abou t one-sixth the pretreatment level in the 12th month, Because the seru m level of 1,5-anhydro-D-glucitol continued to decline, falling below the limit at which its renal reabsorption is normally activated, this decrease did not seem to be caused directly by a nutritional deficienc y of this substance. 3. The urinary excretion of 1,5-anhydro-D-glucito l was closely correlated (r = 0.792) with that of N-acetyl-D-glucosami nidase; but not with the serum creatinine level or of the urinary excr etion of micro-albumin or of urinary beta(2)-microglobulin, We observe d no glucosuria, hyperuricuria or changes in serum electrolytes during total parenteral nutrition. 4. The reduction in the serum level of 1, 5-anhydro-D-glucitol and the urinary excretion of N-acetyl-beta-glucos aminidase were correlated with the duration of total parenteral nutrit ion administration. 5. Thus, the long-term administration of total par enteral nutrition (free of 1,5-anhydro-D-glucitol) appeared to induce a degree of renal tubular dysfunction as shown by the reabsorption of 1,5-anhydro-D-glucitol and the excretion of N-acetyl-beta-glucosaminid ase, These results suggest there exists a unique carrier system for 1, 5-anhydro-D-glucitol.