An Overview of Molecular Mechanism of Nephrotic Syndrome

Overview

Journal Int J Nephrol

Publisher Wiley

Specialty Nephrology

Date 2012 Jul 31

PMID 22844593

Citations 12

Authors

Juliana Reis Machado

Laura Penna Rocha

Precil Diego Miranda de Menezes Neves

Eliangela de Castro Cobo

Marcos Vinicius Silva

Lucio Roberto Castellano

Rosana Rosa Miranda Correa

Marlene Antonia Reis

Affiliations

Soon will be listed here.

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.

Citing Articles

Detailed Pathophysiology of Minimal Change Disease: Insights into Podocyte Dysfunction, Immune Dysregulation, and Genetic Susceptibility.

Roman M, Nowicki M Int J Mol Sci. 2024; 25(22).

PMID: 39596249 PMC: 11595011. DOI: 10.3390/ijms252212174.

Dissociation Phenomenon of Erythrocyte Agglutination and Its Application to Assay of Functional Activity of the Complement System in Clinical Laboratory.

Ding X, Liu L, Yang G, Liu H J Clin Lab Anal. 2024; 38(6):e25028.

PMID: 38506373 PMC: 10997817. DOI: 10.1002/jcla.25028.

In situ evaluation of podocytes in patients with focal segmental glomerulosclerosis and minimal change disease.

da Silva C, Dos Reis Monteiro M, Araujo L, Urzedo M, Rocha L, Dos Reis M PLoS One. 2020; 15(11):e0241745.

PMID: 33147279 PMC: 7641434. DOI: 10.1371/journal.pone.0241745.

Protosappanin-A and oleanolic acid protect injured podocytes from apoptosis through inhibition of AKT-mTOR signaling.

Zheng J, Zhang S, Chen H, Cai X, Zhang C, Li S Cell Biol Int. 2019; 44(1):189-199.

PMID: 31441181 PMC: 6973098. DOI: 10.1002/cbin.11218.

Evaluation of the Diagnostic Potential of uPAR as a Biomarker in Renal Biopsies of Patients with FSGS.

da Silva C, Araujo L, Dos Reis Monteiro M, Pereira L, da Silva M, Castellano L Dis Markers. 2019; 2019:1070495.

PMID: 31191741 PMC: 6525920. DOI: 10.1155/2019/1070495.

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