Why do children with recurrent IgA nephritis?

As people of IgA nephritis deepening of the study, in understanding, especially children with IgA nephritis IgA nephritis has undergone significant changes, especially genetics research progress, no longer will IgA nephritis as a separate disease entity view, the clinical symptoms of the disease type, pathological or disease progression rate complicated by multiple genetic factors and often the result of repeated attacks, unhealed for many years. Renal biopsy poor prognosis factors: a glomerular sclerosis, interstitial fibrosis, glomerular capillary is violated, diffuse hyperplasia and diffuse crescent formation.
Kidney experts after years of clinical observation and in-depth validation of the pathological analysis, we found IgA nephritis renal fibrosis in the occurrence, development and prognosis plays a major role, does not turn it as a "separate disease entity to look at." Currently worldwide are also at different levels of theory study on renal fibrosis.
In pathological analysis, IgA nephritis is mainly IgA antibodies or immune complex deposition in the glomeruli mesangial area, leading to mesangial cell damage, which can lead to inflammation. Massive proliferation of mesangial cells or shrink, resulting in microcirculation, leading to ischemia and hypoxia. Due to ischemia, hypoxia resulted in substantial renal capillary endothelial cells, epithelial cells, renal interstitial fibroblast cell damage, and the occurrence of phenotypic transformation, the formation of renal fibrosis; because of damaged endothelial cells or epithelial cells leaving basement membrane and the charge barrier function change, resulting in a lot of protein and red blood cell leakage, the formation of urinary protein, hematuria. The reason why children IgA nephritis with hematuria, proteinuria and other symptoms that renal epithelial cells are damaged, the basement membrane and the charge barrier function is changed, the emergence of hematuria, urinary protein.
The contents of that kidney disease urine protein and erythrocyte leakage, mainly by glomerular filtration membrane damage caused by increased permeability caused. At present, if only corticosteroids, Hook, cyclophosphamide suppress IgA-based antibody and immunoglobulin production, it can only be for primary disease treatment; does not clear the deposition of IgA receptors and immune complexes, can not improve renal ischemia and hypoxia in the state, it can not be completely eliminated due to the treatment and mesangial cell damage caused by a series of reactions, the more can not effectively repair glomerular filtration membrane, to restore its normal filtration function.
Thus, the use of steroids, cyclophosphamide, or simply because of a momentary triptolide suppressed the generation of various types of receptors, and sometimes control the "inflammatory" response and progress of the damage, leaving the urine protein, occult blood in a period of time to reduce or even disappear . But it does not address the fundamental cause of the drug after the disappearance, or induced for some reason, urine protein, occult blood will come back!
All in all, if the child can not get a good Iga nephritis treatment at an early stage, then, when IgA nephritis sent to renal insufficiency or uremia stage of development is even more the outcome of renal fibrosis. Therefore, they need timely blocking renal fibrosis in the development process, in order to prevent kidney was replaced by scar tissue, thereby protecting children remaining renal function.