On basic research in FSGS progress include

A plasma induced nephropathy factor previous evidence that the glomerular permeability factor is one of the reasons leading to FSGS, but has not clarified its essence. Infusion to rats with FSGS patient plasma, or serum extracts of staphylococcal protein A column can cause proteinuria. The extract of thermal instability, protease-sensitive, molecular weight of about 30 to 50 kDa, Podocytes in vitro incubation in plasma of patients with nephrotic syndrome enable podocytes of nephrin, podocin in and CD2AP molecules from the membrane translocation to the cytoplasm. Another study showed that normal human plasma in the plasma of patients with this role can be fully eliminated. Some scholars believe that there are protective factors in normal human plasma of FSGS patients lack the factor disease. The plasma in the end the existence of of FSGS protection molecules or pathogenic factor has not been fully elucidated.
The pathogenic role of podocytes in FSGS pathogenesis of podocytes gradually become the focus, the number of podocytes reduction is the main mechanism leading to glomerular sclerosis. The current positioning the podocyte hole membrane-associated molecules include: ① NPHS1 gene, the gene mutation is a major cause of nephrotic syndrome, Finnish type (CNF), and is mainly composed of two mutations (Fin major and Fin minor) due to massive proteinuria in NPHS1 gene knockout mice, their encoding nephrin molecules are also involved in enough cell signal transduction, including activation of the MAPK signaling pathway; ② The NPHS2 gene encoding podocin molecules can interact with nephrin and CD2AP may have a connection function of the gene mutation can lead to autosomal recessive inheritance of FSGS; ③ carrying CD2AP and its, it is located within the podocyte adapter molecules combine with the intracellular domain of the CD2 molecule, and nephrin anchored in the cytoskeleton, carrying CD2AP and its gene knockout mice manifested as nephrotic syndrome and renal insufficiency; ④ The ACTN4, which encodes the alpha-Actinin-4 is a muscle dynamic protein filaments cross-linked protein, is an important part of foot processes, to the maintenance of the skeleton of podocytes complete very important, ACTN4 gene mutations can cause autosomal dominant inheritance of FSGS, the ACTN4 knockout mice exhibit proteinuria and renal insufficiency; ⑤ The TRPC6, it encodes a calcium ion flow channel, TRPC6 gene mutations result in autosomal dominant genetic of FSGS.Found multiple mutations have contributed to the increase in calcium influx may therefore TRPC6 gene mutation as a functional (gain of function) pathogenic; ⑥ The PLCE1 gene, the gene mutation can lead to diffuse mesangial hyperplasia and FSGS lesions, thegene knockout zebrafish nephrotic syndrome.