Abstract
Collapsing glomerulopathy (CG) represents a morphologic pattern of disease, characterized histologically by glomerular capillary collapse, severe podocyte injury, and glomerular epithelial cell proliferation, and clinically by marked proteinuria and renal insufficiency. CG has multiple etiologies; however, many questions remain about its pathogenesis. A new set of animal models of CG, characterized by absence of the normal podocyte cytoskeletal protein alpha-actinin-4, has potential to help us gain a greater understanding of cellular events involved in producing this pattern of disease.
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