Diabetic damage of selective renal reabsorption assessed by albumin negative charge

To clarify the pathogenesis of diabetic albuminuria at its onset, the percentage of glycated albumin (%G-albumin) in excreted urinary albumin and its negative charge were assayed. In non-diabetic albuminuria (control-A) group, the high ratio of urinary %G-albumin to serum %G-albumin (urine/serum ratio of %G-albumin) suggested a selective renal excretion of glycated albumin (G-albumin) over albumin as a result of normally-functioning selective reabsorption of albumin over G-albumin in renal tubules. Urinary %G-albumin and albumin negative charge indexing the degree of glycation, which was assayed by the binding capacity of positively-charged Alcian Blue (ABBC), thus negatively correlated with serum %G-albumin. In non-insulin dependent diabetic subjects with albuminuria (DM-A), however, urinary %G-albumin and ABBC positively correlated with serum %G-albumin, and the urine/serum ratio of %G-albumin was low and gradually increased toward 1 as serum %G-albumin increased. Although the strict glycemic control for 3 weeks reduced the increased urinary %G-albumin and ABBC, the decreased urine/serum ratio of %G-albumin remained unaltered. It is concluded that hyperglycemia-induced renal damage starts with the loss of selective tubular reabsorption of albumin over G-albumin, and that this damage cannot be recovered by strict glycemic control for 3 weeks.