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In the early stages of DKD, increased hyper-reabsorption and gluconeogenesis expose proximal tubular cells to hypoxia, resulting in mitochondrial dysfunction, increased oxidative stress and tubular injury ( Mitochondria is the primary organelle of in PTECs that is modulated to oxidative stress and hypoxic injury in the diabetic state ( Although there are a large number of in vitro and in vivo studies investigating the mechanism of hypoxia-induced renal tubular damage, due to the lack of non-invasive means, there are few clinical studies that have evaluated renal hypoxia in detail
Plast Reconstr Surg
Conservative avoidance deserves serious consideration in this group
Accessed August 31, 2013
Hyporesponsiveness to erythropoiesis stimulating agents in chronic kidney disease: the many faces of inflammation
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