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 rat...
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Published in | Diabetes research and clinical practice Vol. 33; no. 3; pp. 181 - 189 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Shannon
Elsevier Ireland Ltd
01.08.1996
Elsevier Science |
Subjects | |
Online Access | Get full text |
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Summary: | 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. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0168-8227 1872-8227 |
DOI: | 10.1016/0168-8227(96)01296-X |