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- W1486923466 abstract "The pathophysiology of diabetic nephropathy is complex and incompletely understood. Several mechanisms (e.g., hemodynamic changes, fibrosis, hypoxia, oxidative stress, and inflammation) and various mediators, including advanced glycation end products (AGEs) and transforming growth factor-β1, act in concert and contribute to the progression of diabetic nephropathy. Furthermore, the different renal cell types (mesangial cells, podocytes, tubular epithelial cells, endothelial cells, and fibroblasts) undergo pathological changes and are therefore involved, via “crosstalking,” in kidney tissue destruction and subsequently loss of renal function. Some insight has been gained from analysis of biopsies from patients with diabetic nephropathy, but most information about the pathophysiology of diabetic nephropathy is gathered from animal models." @default.
- W1486923466 created "2016-06-24" @default.
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- W1486923466 date "2012-12-17" @default.
- W1486923466 modified "2023-09-24" @default.
- W1486923466 title "Pathophysiology of Diabetic Nephropathy" @default.
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- W1486923466 doi "https://doi.org/10.1002/9781118494073.ch4" @default.
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