Prolonged hyperalimentation as a possible cause of renal tubular dysfunction: evaluation of 1,5-anhydro-D-glucitol resorption and N-acetylglucosaminidase excretion in humans.

1. A major polyol found in the sera and other tissues of humans, 1,5-anhydro-D-glucitol, is mainly ingested in the diet and is excreted in urine. We compared the influence of the long-term administration of total parenteral nutrition free of 1,5-anhydro-D-glucitol with that of total 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 concentration of 1,5-anhydro-D-glucitol and its kinetics remained unchanged in the 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 about one-sixth the pretreatment level in the 12th month. Because the serum 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 deficiency of this substance. 3. The urinary excretion of 1,5-anhydro-D-glucitol was closely correlated (r = 0.792) with that of N-acetyl-beta-glucosaminidase; but not with the serum creatinine level or of the urinary excretion of microalbumin or of urinary beta 2-microglobulin. We observed 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-glucosaminidase were correlated with the duration of total parenteral nutrition administration.(ABSTRACT TRUNCATED AT 250 WORDS)