Glomerulonephritis.

Abstract

Advances in cell and molecular biology have generated fresh insights into the mechanisms of glomerular injury, a field with very few substantial advances in the past 20 years. Currently, the nature of renal antigens involved in the immune reaction is being identified, as in the case of Goodpasture antigen. Many recent studies focus on T-cell and macrophage functions in glomerulonephritis that initiate acute inflammatory events and determine glomerular disease progression. Recent data established that after inflammatory cell migration to the glomerulus, subsequent damage depends on cell adhesion to cytokine-activated endothelial cells, a process mediated by a variety of specialized molecules. It seems easy to predict that within the next few years these studies will have a major impact on the way these diseases are treated. Already, evidence indicates that, in experimental animals, monoclonal antibodies blocking adhesive molecules prevent or reduce glomerular damage. Cytokines and growth factors, by promoting resident cell proliferation and modulating extracellular matrix synthesis and metabolism, modulate acute glomerular injury and subsequent scarring. Recent studies have established that glomerular injury is related to urinary protein excretion, an issue that has been approached in humans by combining studies on barrier size selectivity with morphometry. An emerging concept suggests that leaking of proteins through the glomerular capillary has an intrinsic renal toxicity that is likely due to proximal tubular over-reabsorption of the abnormally filtered macromolecules. Data are also accumulating that may soon link the degree of tubulointerstitial injury with glomerular damage and subsequent development of renal scarring.