Renal pathology in diabetes mellitus.
The key change in diabetic glomerulopathy is accumulation of extracellular material. Basement membrane thickening and matrix expansion develop concomitantly. In insulin-dependent diabetic patients persistent microalbuminuria is associated with an early stage of glomerulopathy. Albuminuria in non-insulin-dependent patients does not always reflect glomerulopathy. Renal and glomerular hypertrophy in the early stages of insulin-dependent diabetes mellitus is unlikely to play a dominant role in the development of glomerulopathy. Loss of capillary surface, closely associated with loss of glomerular function, is only partly explained by mesangial expansion--glomerular occlusion plays an important role. Possible mechanisms of albuminuria are qualitative changes of the basement membrane, eg, loss of proteoglycans and excess glycosylation; epithelial cell changes; new vessel formation; remodeling of glomerular structures; and impeded function of juxtaglomerular arterioles. The interplay among abnormalities in individual compartments of the diabetic kidney should be explored.
Osterby
R
R
Electron Microscopy Laboratory, Institute of Pathology, Kommunehospitalet, Arhus C, Denmark.
D000818:Animals; D003920:Diabetes Mellitus / Q000473:pathology*; D003928:Diabetic Nephropathies / Q000473:pathology*; D005921:Glomerulonephritis / Q000473:pathology; D006801:Humans; D007668:Kidney / Q000473:pathology*