[The relation between the changes of width and anionic sites of glomerular basement membrane and transferrinuria in rats].
The changes of width and anionic sites of glomerular basement membrane (GBM) are considered early changes of diabetic nephropathy. Recent work suggests that the normal barrier to the penetration of renal glomerular basement membrane by anionic plasma proteins may depend in part on the existence of negatively charged sites within the membrane. We evaluated the relationship between the change of width, anionic sites of GBM and transferrinuria in diabetic rats and normal controls in 1, 3, 6 months after administration by STZ. Diabetic rats revealed a thicken GBM (0.40-0.44microns) and reduced anionic sites (16-12/1000nm GBM length) compared with control rats (0.22 microns, 20-22/1000 nm GBM lenth). Transferrinuria was also significantly greater in diabetic rats than normals (P < 0.01). The changes in anionic sites and transferrinuria represented defect of GBM charge barrier in early phase of diabetic nephropathy. Aminoguanidine attenuated the rise in transferrinuria and prevented GBM thickness and loss of anionie sites.
Chen
Y
Y
Department of Endocrine, First Hospital, Beijing Medical University.
Qian
Y
Y
D000818:Animals; D001485:Basement Membrane / Q000648:ultrastructure; D003921:Diabetes Mellitus, Experimental / Q000473:pathology; D003928:Diabetic Nephropathies / Q000473:pathology* / Q000652:urine; D007678:Kidney Glomerulus / Q000648:ultrastructure*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D014168:Transferrin / Q000652:urine*
D014168:Transferrin