title: Morphological studies on the kidney of the spontaneous nephrotic (ICGN) mice in the late stage.
abstract: Spontaneous nephrotic (ICGN) mice develop proteinuria, hypoproteinemia and hypercholesterolemia. These symptoms steadily progress to chronic renal failure. Details of the changes of the kidney, in the late stage (more than 5 months old) were investigated by both light and electron microscopy. The kidney exhibited a slightly whitish, granular surface and the cortex became thinner and contained fibrous lesions, in which clusters of unaffected and occluded renal tubules were randomly scattered. In the juxtamedullary and outer medullary zone, there were highly dilated renal tubules, which sometimes contained urinary casts. The glomerulus exhibited basement membrane thickening in the capillary loops and the capillary lumen was narrowed in size and sometimes occluded. No detachment of the podocyte from the basement membrane was observed and the podocyte foot-processes were extensively fused, causing their characteristic slits to be lost. The thickened basement membranes were found both in the glomerulus and around the occluded renal tubules, while the basement membrane in the dilated renal tubule appeared normal. Therefore, the basement membranes of the glomerulus and renal tubules appear to react differently in the pathogenesis of the condition. In conclusion, ICGN mice are a good model for not only the nephrotic syndrome but also for chronic renal failure.
authors.affiliation: Department of Anatomy, Sapporo Medical University School of Medicine, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Tatsumi
authors.forename: S
authors.initials: S
authors.lastname: Satoh
authors.forename: M
authors.initials: M
authors.lastname: Okamoto
authors.forename: M
authors.initials: M
authors.lastname: Nakamura
authors.forename: T
authors.initials: T
authors.lastname: Asano
authors.forename: T
authors.initials: T
authors.lastname: Kurosawa
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D007668:Kidney / Q000648:ultrastructure*; D007676:Kidney Failure, Chronic / Q000473:pathology*; D051379:Mice; D008813:Mice, Inbred ICR / Q000235:genetics; D008854:Microscopy, Electron; D009404:Nephrotic Syndrome / Q000473:pathology*; D011507:Proteinuria / Q000209:etiology