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A large number of pro-inflammatory factors such as interleukins IL-6, IL-8, IL-1, monocyte chemoattractant protein-1(MCP-1), ROS and T cell activation secretion regulator can infiltrate into the renal capsule from an abnormal glomerulus and destroy the function of the renal tubules ( Hyperglycemia, AGEs, mitochondrial oxidative stress and ultrafiltration cytokines act on renal tubular cells and trigger multiple cellular pathways such as PKC-, -, and -, NF-B, P38 and ERK1/2 pathways, further exacerbating renal tubular cell hypertrophy, apoptosis, and accumulation of tubulointerstitial inflammatory factors ( in vitro study has shown that high glucose induces the expression of TLR4 in PTECs through the activation of PKC, resulting in the upregulation of CCL-2 and IL-6 expression

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