Figures & data
Figure 1. Autophagy insufficiency is associated with the pathogenesis of podocyte injury and massive proteinuria in diabetic nephropathy. Diabetes alone results in the development of mild glomerular lesions, such as glomerular hypertrophy, basement membrane (GBM) thickening, mild mesangial expansion and minimal proteinuria, leading to slowly-progressive renal dysfunction. However, the combination of insufficient podocyte autophagy and diabetic conditions results in podocyte loss, foot process alterations and lysosome dysfunction. This results in massive refractory proteinuria and a rapid decline of renal function. Autophagy insufficiency-related podocyte loss may be involved in the "point of no return" in diabetic nephropathy.
![Figure 1. Autophagy insufficiency is associated with the pathogenesis of podocyte injury and massive proteinuria in diabetic nephropathy. Diabetes alone results in the development of mild glomerular lesions, such as glomerular hypertrophy, basement membrane (GBM) thickening, mild mesangial expansion and minimal proteinuria, leading to slowly-progressive renal dysfunction. However, the combination of insufficient podocyte autophagy and diabetic conditions results in podocyte loss, foot process alterations and lysosome dysfunction. This results in massive refractory proteinuria and a rapid decline of renal function. Autophagy insufficiency-related podocyte loss may be involved in the "point of no return" in diabetic nephropathy.](/cms/asset/74148e13-af11-4848-ac70-811fb47ef89d/kaup_a_1115173_f0001_c.gif)