Membranous glomerulopathy (MGN) is a frequent cause for nephrotic syndrome in adults. In this overview, the basic pathogenic features of Heymann nephritis, a "classical" model of MGN in rats, are compared with those of human MGN. While the pathogenic antigen(s) of rat Heymann nephritis (the polyspecific receptor protein gp330/megalin), and that of human MGN (unknown) are obvioulsy different, the results indicate that the molecular mechanisms of proteinuria may be similar in both instances and involve the formation of lipid peroxidation adducts in the glomerular capillary filter. As a consequence, probucol - an efficient inhibitor of lipid peroxidation - drastically reduces proteinuria both in Heymann nephritis and in a large proportion of human patients with MGN.