Influence of uremic toxins and nonesterified fatty acids on drug and thyroid hormone binding in serum.

respectively. These icodextrin metabolite concentrations were reported to be the maximum reachable concentrations in vivo (2). From each sample, 100 mL was centrifuged and analyzed on a Hitachi 911 with a plasma glucose dehydrogenase (GDH) method (Boehringer Mannheim). The whole blood samples were analyzed using an EML 105 with a glucose oxidase (GOD) membrane method (Radiometer), a Chiron 865 with a GOD membrane method accompanied by a glucose reference electrode, and bedside glucose analyzers: Accutrend Sensor with a bioamperometric GDH method (Boehringer Mannheim), Glucocard Memory with a bioamperometric GOD method (Menarini Diagnostics), Glucotouch with a colorimetric GOD method (Lifescan, Johnson & Johnson), One Touch Profile with a colorimetric GOD method (Lifescan), One Touch II with a colorimetric GOD method (Lifescan), and Precision with a GOD method (Medisense). The results of the samples containing icodextrin metabolites were compared with the blank sample and expressed as a mean difference. Interference was defined as a mean difference .0.5 mmol/L (Table 1). The icodextrin metabolites showed no interference in glucose measurements by the Hitachi 911 and the Chiron 865 analyzer. The EML 105 system showed a positive interference from maltose but no interference from maltotriose or maltotetraose. The bedside glucose analyzer Accutrend Sensor showed a considerable positive interference from all three icodextrin metabolites. The Glucocard Memory showed positive interference with maltose and maltotriose in one sample; for the other sample, it registered a result of “LO” (,2.2 mmol/L). The Glucotouch and the One Touch Profile showed no interference with any of the metabolites. The One Touch II showed a positive interference for maltotriose and maltotetraose. The Precision showed an interference with maltose in one sample and slight interference with maltotriose and maltotetraose in another sample. The interference was related to the concentration of the interferent, regardless of the glucose concentration of the sample. In conclusion, the icodextrin metabolites may cause erroneously high glucose results, depending on the analysis system used. The clinically significant effect of interference by icodextrin metabolites is the potential risk of missing the diagnosis of hypoglycemia. Moreover, in diabetic patients undergoing icodextrin-CAPD therapy, the observed icodextrin metabolite interference may lead to unexplainable fluctuations in measured glucose. References 1. Mystry CD, Gokal R. The use of glucose polymer (icodextrin) in peritoneal dialysis: an overview. Perit Dial Int 1994;14(Suppl 3):S158–61. 2. Davies DS. Kinetics of icodextrin. Perit Dial Int 1994;14(Suppl 2):S45–50.