The nature of basal lamina alterations in human diabetic glomerulosclerosis.
Studies of human diabetic glomerulosclerosis with a newly devleoped guanidine method have revealed that, like renal tubules, thickening of the glomerular capillary basal lamina is due exclusively to inordinate accumulation of the epithelial basal lamina. There is no excessive deposition of the endothelial basal lamina. Thus, the diabetic nephropathy is characterized by a diffuse thickening of the epithelial basal lamina involving the entire nephron unit, a feature distinct from peripheral diabetic microangiopathy, where the endothelial basal lamina plays a predominant role. The nodular and diffuse mesangial sclerosis is composed of increased mesangial basal lamina, there is no evidence indicating collapsed capillary epithelial basal lamina within Kimmelstiel-Wilson nodules. Hitherto undescribed alterations in the juxtamesangial epithelial basal lamina suggesting new glomerular capillary tuft formation are also presented.
D002196:Capillaries / Q000648:ultrastructure; D003928:Diabetic Nephropathies / Q000473:pathology*; D004727:Endothelium / Q000648:ultrastructure; D004848:Epithelium / Q000648:ultrastructure; D006801:Humans; D007678:Kidney Glomerulus / Q000098:blood supply / Q000503:physiopathology / Q000648:ultrastructure*; D008854:Microscopy, Electron; D008875:Middle Aged; D009399:Nephrons / Q000648:ultrastructure