Mechanisms underlying idiopathic NS. In both its steroid-sensitive and its steroid-insensitive form, this condition can apparently arise through a T cell dysfunction that leads to the synthesis of a still-unidentified circulating factor that compromises the glomerular permeability barrier. By contrast, in a subset of steroid-resistant NS, the disease is due to a primary defect in the glomerular filtration filter. The potential interactions between this immune defect and altered structural properties of the glomerular epithelium remain highly speculative.