FSGS that continued progress may be

(1) growth factors. The basis put forward this doctrine: ① pathological mild hypertrophy with a small ball with mild sclerosis often coexist. FSGS glomerular volume significantly larger than the minimal change disease or normal controls. ② inhibition of specific growth factors can effectively prevent the development of glomerular sclerosis.For example, an inhibitor of angiotensin Ⅱ by inhibiting platelet-associated growth factors and the transfer of growth factor β treatment of FSGS.③ the clinical lead to poor glomerular proliferation of abnormal factors, including hypoxia, hypertension and renal volume reduction, such as more than a kidney nephrectomy and unilateral renal dysplasia, often accompanied by the hair of FSGS. Molecular biology research from animal models and human biopsy data prompt The glomerulosclerosis each process is controlled by a major and several minor growth factor such as platelet-associated growth factors like early play an important role in hardening transfer growth factor beta hardening severity.
(2) hypertension. Glomerular pressure may impair kidney function and structure. On the contrary, reducing stress can improve and prevent hardening. Some people think that the pressure increased, the increase in capillary diameter, resulting in increased vascular wall tension caused by hardening. However, in the case of diabetic nephropathy and reflux nephropathy, glomerular increases than capillary diameter increased, but the vessel length extension and branch increase in the number; In addition, high blood pressure does not often appear in front of the glomerular sclerosis, as well as the The researchers found that only resection in nephron glomerular volume was significantly increased before the development of hardening. Therefore, high filtration, high perfusion pressure may not glomerular volume increase, or hardening of the only condition.
(3) the role and influence of proteinuria of FSGS progress: Some scholars believe that proteinuria itself may promote glomerular mesangial and epithelial cells or tubulointerstitial renal tissue scarring. Secondly, proteinuria can be induced by the inflammatory mediators, such as macrophages and TGFβ increased, leading to glomerular interstitial scarring.
(4) high cholesterol may affect the progress of FSGS. Foam cells, fat phagocytes with FSGS is more common. Some scholars believe that in the case of proteinuria, the filtered neutral fat matrix aggregation a specific pathogenic role [5,6]. Small lesions of lipids is also very significant and do not necessarily have hardened, it prompts the hyperlipidemia is only the cofactors of the hardening process.