Focal segmental glomerulosclerosis - disease etiology

FSGS has many causative factors . If poisoning injury, humoral and hemodynamic changes , can lead to damage to the capillary wall , so that the macromolecular protein production and retention, after the deposition of immunoglobulin binding C1q and C3 , causing degeneration and podocytes with basement membrane phase out . The study found that the podocyte phenotype changed during primary FSGS. But how epithelial cells of these injuries result in capillary loop collapse and hardening unclear , FSGS may be a manifestation of epithelial lesions after aggravating tissue repair . Focal sclerosis lesions rapidly relapse after kidney transplantation , indicating the presence of systemic factors in the pathogenesis of FSGS . Residual renal hemodynamic changes occurred in the organization caused by compensatory glomerular capillary pressure, high perfusion and high filtration , resulting in damage to the epithelial cells and endothelial cells , mesangial cell dysfunction , leading to progressive focal segmental sclerosis . This pathological process may be aggravated by a high intake of protein , limiting protein intake and blood pressure treatment and relief. Endothelial cell injury induced platelet aggregation and micro-thrombosis , and increased development of lesions ; many FSGS occurs with this pathogenesis , such as " chronic " post- streptococcal glomerulonephritis , and chronic renal allograft rejection, reflux nephropathy and town pain medicine kidney disease. In addition, the observed nearly marrow glomerular glomerular filtration rate is higher than the cortex glomerular hemodynamics is also supported risk factors of FSGS . Drug abuse and AIDS can cause typical FSGS nephrotic syndrome and progressive renal failure, it can be the end result most proliferative glomerulonephritis . However, most cases are idiopathic , is found in the first biopsy histopathologic type was FSGS. In addition to segmental sclerosis seen in FSGS , but also can be the final result of proliferative glomerulonephritis ( glomerulonephritis after infection , such as ) or with high filtration nephrotic syndrome related to some patients after a focal Festival posterior segment of the proliferative phase , segmental necrosis and scar formation , this situation is common in secondary glomerulonephritis .