The glomerular filtration barrier is highly size and charge selective, both podocyte and glomerular basement membrane are essential for permeability. In disease state, with the normal filtration structure broken down, podocytes detach from the glomerular basement membrane. The total number of podocytes decreasing followed by proteinuria. Although the mechanism of podocytes loss is still being debated, adhesion dysfunction is thought to contribute to the decrease in podocyte density. Others have given much attention to podocyte foot process fusion, podocyte apoptosis, and podocyte proliferation disability in the pathological state. This review focuses on the interaction of podocytes with glomerular basement membrane, and the molecules contributing to podocyte detachment. Here we illustrate biology character of the transmembrane matrix receptors integrin ⍺₃β₁, ⍺-/β-dystroglycan, and tetraspanin CD151, we interpret cellular and extracellular transmembrane matrix receptor interrelated proteins. And we summarize the previous research achievement to reveal the internal connections of those proteins and to know how they work together preventing podocyte detachment and then sustaining the normal shape of glomerular filtration barrier.