PubMedDate not supplied
Corticosteroids have multiform effects on traffic and functional capabilities of inflammatory or immunologically reactive cells, on various soluble factors, vascular and tissue responses. There is a different sensitivity of various populations and subpopulations of cells to the corticosteroid modulation. These mechanisms are still under discussion, but the final effects appear to support the use of corticosteroids in a number of idiopathic glomerulonephritis (GN). In the minimal change GN the 10 years after onset survival was not significantly increased by introducing corticosteroids, but the prompt disappearance of proteinuria (80% of adults by 8 weeks in our own series) supported their use. The problem of corticosteroid treatment in the focal sclerosing GN is complicated by the probable coexistence of two histologically undistinguishable forms (one of the these nonsteroid sensitive). In our own series the corticosteroid response, although transient, was present in 44% of 16 patients. We obtained a high number of total remissions (57%) and partial remissions (14%), in membranous GN, where the conflicting data of the literature suggest differences in the criteria of selection and admission of patients to corticosteroid treatment, calling attention to further controlled trials. In rapidly progressive GN the combined use of corticosteroids, immuno suppressants and heparin has elicited a stabilization or improvement of renal function in 40% of the treated patients. By the same treatment we observed a total remission in 19% and a partial remission in 62% of severely nephrotic patients with histological appearance of membranoproliferative GN characterized by massive subendothelial deposits of the early complement fractions (C1, C4). Although it is impossible to draw firm conclusions both on pathogenesis of idiopathic GN or on the biochemical, cellular and tissue effects of corticosteroid, these drugs appear sometimes effective in clinical practice.