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