Using super‐resolution 3D‐structured illumination microscopy, we observed a spatially restricted up‐regulation of the tight junction protein claudin‐5 (CLDN5) in areas where podocyte processes of patients suffering from minimal change disease (MCD), focal and segmental glomerulosclerosis (FSGS) as well as in murine nephrotoxic serum (NTS) nephritis and uninephrectomy DOCA‐salt hypertension models, were locally injured. This evidence concerns the gene CLDN5 and lipoid nephrosis.