Mice deficient in α-actinin-4 have severe glomerular disease
J. Clin. Invest. Claudine H. Kos, et al. 111:1683 doi:10.1172/JCI17988 [Go to this article.]

Figure 4
(a and b) Electron microscopic appearance of kidneys from 10-day-old Actn4^+/+ (a) and Actn4^–/– (b) littermates. (c and d) Kidneys from 5-week-old Actn4^+/+ (c) and Actn4^–/– (d) mice. (e and f) Kidneys from 10-week-old Actn4^+/+ (e) and Actn4^–/– (f) mice. In all cases, Actn4^–/– mice show altered glomerular ultrastructure. In the 10-day-old kidney (b), there is mild disruption of the normal podocyte structure with focal areas of podocyte effacement. The disease is more extensive in the older mice (c and e). (g and h) Early changes in Actn4^–/– mice are shown at higher power. As shown in g, some Actn4^–/– mice demonstrated areas with duplications, or “blebs,” in the GBM on the subepithelial aspect (arrow). These abnormalities were not seen in the control mice, nor were they present in all Actn4^–/– mice. In h, focal areas of foot-process effacement in an Actn4^–/– mouse are evident (arrow).