Prolonged Hyperalimentation as a Possible Cause of Renal Tubular Dysfunction: Evaluation of 1,5-Anhydro-d-Glucitol Resorption and N-Acetylglucosaminidase Excretion in Humans

Abstract

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)

Transient Renal Glucosuria in Patients with Tetanus

“…Hyperalimentation has been claimed to be associated with glucosuria [18], although this has not been a universal finding [19]. This, however, is an unlikely explanation in our patients since none of our cases received such a dietary support.…”

1,5-Anhydroglucitol levels are low irrespective of plasma glucose levels in patients with chronic liver disease

“…In this relation, it has been shown that serum 1,5-AG levels and serum uric acid levels are low in patients receiving prolonged total parenteral nutrition, which may be caused by impaired renal tubular function. 24,25 Furthermore, it is indicated that hypouricaemia in patients with liver cirrhosis improves with recovery of liver function accompanied by decrease in excretion of uric acid. 21 It is intriguing whether serum 1,5-AG levels may increase along with improvement of liver function in these patients.…”

Metabolic and catheter complications of parenteral nutrition

“…Inorganic phosphate decreases urinary calcium losses and may have a therapeutic role [53]. Renal tubular dysfunction may be caused by prolonged TPN [54]. Amino acid loading has been found to disrupt proximal tubular function, and parenteral iron formulations have been associated with renal tubular damage [55].…”