Síndrome nefrótico: mecanismos fisiopatológicos implicados

Abstract

The Nephrotic syndrome (NS) is characterized by massive proteinuria followed hypoproteinemia, hypercholesterolemia, lipiduria, and edema. Glomerular filtration barrier (BFG) is formed by glomerular endothelial cells (GEC), the glomerular basement membrane (GBM) and podocyte foot processes with diaphragm slits between them. The BFG coordinated function has been considered as the main constraint against plasma leakage of protein into the urine. Damage to any of these structures can lead to proteinuria. Studies of clinical and experimental research has revealed multiple factors that can alter the permeability to proteins in the BFG in the SN, as well as providing a greater understanding of the mechanisms involved in the pathogenesis and complications of this syndrome . Recent research on the biology of the podocyte, as well as the identification of mutations in genes expressed by podocytes , have allowed a better understanding of the BFG and the mechanisms leading to the development of proteinuria. The prolonged exposure to albumin is detrimental to podocytes and may contribute to the progressive loss of podocytes in proteinuric renal disease. Endocytosis despodocytes
albumin causes an inflammatory response and induces cell death by apoptosis. Has been shown both in vivo and in vitro, severe proteinuria, such as that seen in NS, it may induce activation inflamasomas in renal tubules, with subsequent tubular injury and the development of progressive tubulointerstitial fibrosis.