The plasma concentration of 1,5-anhydroglucitol, a new clinical marker of glycemic control in diabetic patients, was evaluated as a marker of glycemia in 83 diabetic and nondiabetic patients with end-stage renal disease. Plasma 1,5-anhydroglucitol concentration decreased and correlated inversely with blood glucose, hemoglobin A1c, or fructosamine in 48 diabetic patients with normal renal function. In 13 nondiabetic patients with end-stage renal disease not on dialysis, plasma 1,5-anhydroglucitol concentrations were lower than in 23 healthy subjects (6.22 ± 2.10 vs. 24.20 ± 7.50 μg/ml, respectively). The plasma concentration of 1,5-anhydroglucitol concentration in nondiabetic patients with end-stage renal disease was inversely correlated to the urinary N-acetyl-β-D-glucosaminidase activity (r = -0.634) but not to blood glucose, hemoglobin A1c, or fructosamine. Renal tubular damage may contribute to the low plasma concentration of 1,5-anhydroglucitol in this group. The plasma concentrations of this polyol decreased in both diabetic (4.63 ± 1.08 μg/ml) and nondiabetic patients on hemodialysis (4.71 ± 0.87 μg/ml). In these two groups, there was no correlation between plasma concentration of this polyol and blood glucose, hemoglobin A1c, or fructosamine. The plasma concentration of 1,5-anhydroglucitol decreased after a single hemodialysis session. The results showed that impaired renal function and removal of 1,5-anhydroglucitol by dialysis may contribute to its decreased concentration in patients with end-stage renal disease, but that glycemic control does not. Therefore, we should consider renal function when we use plasma 1,5-anhydroglucitol concentration as a marker of glycemic control in diabetic p