is a kidney disorder that leads to changes and inflammation of the structures inside the kidney that help filter wastes and fluids. The inflammation may lead to problems with kidney function.
to PLA2R, usually of IgG4 subclass, are found in 70-80% of patients with primary membranous nephropathy, bind to conformational epitopes on PLA2R expressed in the glomerular , form immune complexes in situ and induce proteinuria, mostly likely via local activation of complement. The autoimmune response is governed by genes at the HLA-DQA1 locus.
The epidemiologic information concerning chronic renal failure (CRF) in children is scanty, particularly with regard to the less advanced stages of renal impairment that are potentially more susceptible to therapeutic interventions aimed at changing the course of the disease and avoiding end-stage renal disease (ESRD).
The treatment consisted of 1g intravenous methylprednisolone given every 24 hours for three consecutive days, followed by oral steroids at a dose of 0.5 mg/kg/daily for 27 days (Cycle A). After the first monthtreatment was replaced by chlorambucil (0.2 mg/kg/daily) for one month (Cycle B). Cycle A and B were repeated three times, so that the whole treatment lasted 6 months.
To understand the mechanisms whereby proteinuria is prevented in the healthy situation, with a focus on the two highly specialised cell types that make up the filtration barrier in the glomerulus; the glomerular epithelial cell or podocyte and the cell (GEnC) that lines the glomerular capillary wall, how they communicate with eachother and how this may change in disease.