[Clinical pathology of the glomerulus--from phenomenon to entity. The membranous lesion].

Characteristics of the membranous lesion are usually the capillary wall thickening in morphology and the clinical manifestation of a nephrotic syndrome. As entities of such a lesion the following types of glomerulonephritis (GN) could be considered: (peri-) membranous GN, garland type of postinfectious GN, and membranoproliferative (MP) GN. The morphological, especially the electronmicroscopical observations relative to separate immune deposit locations in the capillary wall--subendothelial, intramembranous, subepithelial--are the basis to differentiate the diseases as entities. The characteristic finding of the (peri-) membranous GN is the presence of subepithelial immune deposits along the capillary walls, which are separated by "spikes" and later on are incorporated into the basement membrane, while some of the deposits became rarefied; on the other hand, new subepithelial deposits can be observed when the disease of the most common idiopathic form starts again after a period of remission.--The deposits of the garland type of the postinfectious GN--the disease is more often a chronic progressive process than the other types of postinfectious GN--are in a subepithelial location. In contrast to the former the deposits vary in size and number and only some capillary walls are affected.--In type I of the MPGN the immune deposits are located mainly in a subendothelial position, often together with a mesangial interposition in such a manner, that the capillary wall has the appearance of "double contour" histologically. The most striking change of type II is the presence of dense deposits in the lamina densa of the capillary basement membrane ("dense deposit GN"). In type III of MPGN the deposits are located in all three positions of the capillary wall--subendothelial, intramembranous, subepithelial--and the lamina densa is markedly disrupted (little or no affinity for silver in thin sections after silver impregnation). Concerning the entity of the 3 types of MPGN, the depression of serum complement and the complement activating C3-nephritis factor are persistent features of type II, while these findings are obvious only in 50% of type I and III-diseases.