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• W1966235931 abstract "Diabetic kidney disease is a major public health problem. There has been a continual rise in the number of patients with chronic kidney disease and epidemic increases in the number of patients progressing to end-stage renal disease necessitating dialysis and transplantation [ [1] www.usrds.org. United States renal data survey. 2010. Google Scholar ]. Patients with diabetes who develop kidney disease have decreased quality of life and shorter life spans (because of increased morbidity and mortality from cardiovascular disease). In addition, there is a significant cost to society as illustrated by the fact that about 6.5% of the Medicare budget is directed to the end-stage renal disease population that comprises about 500 000 people according to 2009 statistics [ [1] www.usrds.org. United States renal data survey. 2010. Google Scholar ]. There have been many advances in the management of diabetic kidney disease. Yet despite these treatments, the number of cases of diabetic kidney disease continues to rise [ [1] www.usrds.org. United States renal data survey. 2010. Google Scholar ]. Hence, there are very compelling reasons to better understand the mechanisms underlying diabetic kidney disease to develop new treatments that can both prevent the development of kidney disease and slow or stop progression of diabetic kidney disease. As with all complications of diabetes, hyperglycemia activates a series of changes that lead to glomerular and tubular dysfunction and accelerates glomerular cell apoptosis [ [2] Lewko B. Stepinski J. Hyperglycemia and mechanical stress: targeting the renal podocyte. J Cell Physiol. 2009; 221: 288-295 Crossref PubMed Scopus (63) Google Scholar ]. In the following, a brief survey is presented of the various mechanisms that have been attributed to mediate hyperglycemia's adverse effects. More importantly, we will suggest changes in the relative importance of mechanisms that cause diabetic nephropathy by elevating the importance of endogenous protective factors that need to be induced using therapeutic means. Attenuation of diabetic nephropathy in diabetes rats induced by streptozotocin by regulating the endoplasmic reticulum stress inflammatory responseMetabolism - Clinical and ExperimentalVol. 60Issue 5PreviewThe endoplasmic reticulum (ER) is capable of sensing metabolic and stress parameters and integrating intra- and extracellular signals to support a coordinated cell response. In the present study, we verified the hypothesis that 4-phenylbutyric acid (4-PBA), a chemical chaperone, prevented the progression of diabetic nephropathy (DN). Male Sprague-Dawley rats were randomly divided into 3 groups: a normal control group, a DN group, and a DN model plus 4-PBA treatment group (PBA). The DN model was induced by injection of streptozotocin with uninephrectomy. Full-Text PDF" @default.
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• W1966235931 date "2011-05-01" @default.
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• W1966235931 title "A complex interplay of factors causes diabetic nephropathy" @default.
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• W1966235931 doi "https://doi.org/10.1016/j.metabol.2010.10.004" @default.
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