FIG. 6.

Analysis of kidney formation and function from nidogen-deficient embryos and neonates. Hematoxylin-and-eosin-stained sections of kidneys of control (A) and nidogen double-null (B) mice at P0 are shown. Most nidogen-deficient mice formed kidneys that were histologically normal, and immunostaining for laminin γ1 (C, control; D, nidogen double-null mutant) showed a characteristic linear pattern in the glomerulus and under most tubules. Electron microscopy of kidney at E18.5 revealed a normal glomerulus with the typical dual basement membrane being present and in tight contact with the overlying podocytes (e, glomerular epithelial cell; p, podocyte) in control littermates (E) and nidogen double-null embryos (F). However, the tubular basement membrane was often thickened, discontinuous, or even absent (arrows) in double-null kidneys (H), whereas in control kidneys (G), the tubular basement membrane is present (arrows). t, tubular epithelial cell. Bars, 200 μm (A and B), 50 μm (C and D), and 0.25 μm (E to H). Urine removed from the bladders of littermates shortly after birth was analyzed by polyacrylamide gel electrophoresis, and the gels were scanned (I, double-null mutant; K, control). There was a marginal increase in lower-molecular-weight components in the urine of nidogen double-null mice.