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In summary, the literature predominantly aligns with Level 2 and Level 3 evidence, reflecting a considerable degree of scientific rigour
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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
