is characterized by excessive accumulation of glomerular basement membrane and mesangial matrix.
Pathogenesis of the podocytopathy and proteinuria in diabetic glomerulopathy
Figure 2 shows a light microscopic examination of kidneys from diabetic animals revealing diabetic glomerulopathy
characterized by thickening of the glomerular basement membrane, mesangial matrix expansion, arteriolar hyalinosis, and large hyaline proteinaceous droplets (arrow) within the glomeruli (H&E, 200x), occluding capillary loops and attached outside the Bowman's capsule.
Capillaries are variably thickened as compared with the uniform thickening seen in diabetic glomerulopathy
The diagnosis of diabetic kidney disease (DKD) can usually be made with careful clinical and laboratory assessment, but kidney biopsy might be required to prove the presence of diabetic glomerulopathy
The key changes in diabetic glomerulopathy
is thickening of the basement membrane, mesangial cell hypertrophy and accumulation of mesangial matrix (Kimmelstiel-Wilson nodules).
Structural and functional changes in diabetic glomerulopathy
Course of glomerular filtration rate in albuminuric type-2 diabetic patients with or without diabetic glomerulopathy
Taken together, these results indicate that Cnidii rhizoma and Tabanus inhibit the high glucose-induced GMC proliferation partially through suppressing the ECM accumulation and TGF-[beta]1 production, suggesting that these medicines may be a promising agent for treating the development and progression of diabetic glomerulopathy
For example, question 2*4 assumed a basic knowledge of histologic and ultrastructural characteristics of diabetic glomerulopathy
(diabetic patient with a transplanted kidney).
In contrast, several studies report that diabetic patients without retinopathy may have diabetic glomerulopathy
or nephropathy at a rate of 44 to 70%, indicating that the possibility of DN cannot be excluded confidently by the absence of diabetic retinopathy, although the absence of retinopathy strongly favors NDRD.