title: An overview of molecular mechanism of nephrotic syndrome.
abstract: Podocytopathies (minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS)) together with membranous nephropathy are the main causes of nephrotic syndrome. Some changes on the expression of nephrin, podocin, TGF-β, and slit diaphragm components as well as transcription factors and transmembrane proteins have been demonstrated in podocytopathies. Considering the pathogenesis of proteinuria, some elucidations have been directed towards the involvement of epithelial-mesenchymal transition. Moreover, the usefulness of some markers such as TGF-β1, nephrin, synaptopodin, dystroglycans, and malondialdehyde have been determined in the differentiation between MCD and FSGS. Experimental models and human samples indicated an essential role of autoantibodies in membranous glomerulonephritis, kidney damage, and proteinuria events. Megalin and phospholipase-A2-receptor have been described as antigens responsible for the formation of the subepithelial immune complexes and renal disease occurrence. In addition, the complement system seems to play a key role in basal membrane damage and in the development of proteinuria in membranous nephropathy. This paper focuses on the common molecular changes involved in the development of nephrotic proteinuria.
authors: Pathology Laboratory, Department of Biological Sciences, Federal University of Triângulo Mineiro, 38025-180 Uberaba, MG, Brazil.
authors: Juliana Reis
authors: JR
authors: Machado
authors: Laura Penna
authors: LP
authors: Rocha
authors: Precil Diego Miranda de Menezes
authors: PD
authors: Neves
authors: Eliângela de Castro
authors: Ede C
authors: Cobô
authors: Marcos Vinícius
authors: MV
authors: Silva
authors: Lúcio Roberto
authors: LR
authors: Castellano
authors: Rosana Rosa Miranda
authors: RR
authors: Corrêa
authors: Marlene Antônia
authors: MA
authors: Reis