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 albumi n and its negative charge were assayed. In non-diabetic albuminuria (c ontrol-A) group, the high ratio of urinary %G-albumin to serum %G-albu min (urine/serum ratio of %G-albumin) suggested a selective renal excr etion of glycated albumin (G-albumin) over albumin as a result of norm ally-functioning selective reabsorption of albumin over G-albumin in r enal 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 alb uminuria (DM-A), however, urinary %G-albumin and ABBC positively corre lated with serum %G-albumin, and the urine/serum ratio of %G-albumin w as low and gradually increased toward 1 as serum %G-albumin increased. Although the strict glycemic control for 3 weeks reduced the increase d urinary %G-albumin and ABBC, the decreased urine/serum ratio of %G-a lbumin 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 s trict glycemic control for 3 weeks.