What Do I Need to Worry About with IgA Nephropathy Class IV
Latest survey: abnormal increase itself rather than the amount of IgA IgA antibody molecular structure of IgA nephropathy (kidney disease IgA) patients. Healthy human kidney transplant to IgA nephropathy patients, also suffering from the same a few years later IgA nephropathy.
Renal fibrosis played a considerable affect the efficacy of the pathogenesis of kidney patients in the IGA.
First, because the abnormal immune deficiency mucosal IgA nephropathy patients or IgA1 molecular structure, immune complex deposition in the mesangial area or glomerular capillary wall mesangial cells directly cause damage.
Mesangial cell damage after generation changes as follows: contraction and proliferation. Mesangial cell contraction after less variable glomerular filtration area, lower filtration fraction, resulting in glomerular capillary blood disorders, microcirculation blocked, causing further glomerular ischemia and hypoxia, and thus can impaired glomerular capillary endothelial cells. Capillary endothelial cell damage, attracting inflammatory cells, so that the release of inflammatory mediators, and then start the process of renal fibrosis. At this stage in the pathogenesis of inflammation may exhibit, increased mesangial cells, mesangial matrix increase.
GBM pathogenesis produce changes: larger pore filtration or atresia, or basement membrane rupture; charge barrier damaged filtration membrane permeability enhancement. Exhibit clinically occult blood, proteinuria PRO. Continued development and evolution, and gradually developed into glomerulosclerosis.
