Pathogenesis of oedema in nephrotic syndrome: role of epithelial sodium channel

Abstract

Nephrotic syndrome is associated with avid sodium retention, leading to the development of oedema and ascites. Studies in experimental animals suggest that sodium retention in nephotic syndrome is due to increased sodium re-absorption in the collecting duct, which is also the action site of vasoregulatory hormones. However, the mechanisms underlying sodium retention in nephrotic syndrome are incompletely understood and the molecular basis remains undefined. This review summarizes recent insight into the role of epithelial sodium channels (ENaC) in animal models of nephrotic syndrome induced by puromycin aminonucleoside - or HgCl(2) treatment. The sodium retention associated with nephrotic syndrome is caused by increased sodium re-absorption in the aldosterone-sensitive distal nephron segments including the connecting tubule and collecting duct, in which an increased apical targeting of ENaC subunits also plays an important role in the development of sodium retention in nephrotic syndrome.