The pathogenesis of kidney cancer has not been fully elucidated. According to current studies, renal cancer is a malignant tumor with a unique pathogenesis and an extremely complex mechanism of occurrence. The molecular mechanism of its pathogenesis involves the VHL tumor suppressor complex, which loses its function due to genetic mutations, allowing the accumulation of downstream hypoxia-inducible factors (HIF1α, HIF2α), resulting in the overexpression of proteins such as vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF). After binding to the corresponding receptors, VEGF acts on vascular endothelial cells leading to increased vascular permeability, and PDGF acts on outer membrane cells, fibroblasts or vascular smooth muscle cells leading to angiogenesis, both of which promote cell survival, proliferation and migration, eventually leading to kidney cancer and playing an important role in the development and progression of metastatic kidney cancer (MRCC).