These findings indicate that RasGRP4 promoted IL-17 signaling pathway activation in HK-2 cells triggered by the interaction between M1 macrophages and CD4+ T cells during HH/R injury, accelerating the process of tubular injury and fibrosis, with hyperglycemia serving as an important factor that aggravated the immunoinflammatory injury of hypoxia-reoxygenated renal tubules. Here, IL17A is linked to Hyperglycemia.