the role of oxidative stress in hypoalbubimenia nephropathy related to nephrotic syndrome: a critical review

Nephrotic syndrome (ns) is defined as severe proteinuria that results in low ‎albumin levels, increased permeability within the glomerular filtration barrier, and functional ‎impairment. oxidative stress and inflammation are believed to play a significant role in the ‎development of nephropathy. reactive oxygen species, mitochondria, nitric oxide (no) ‎synthases, and xanthine oxidases are all injured by kidney-inducing substances.‎ this study aimed to elucidate the mechanism of hypoalbuminaemia in nephrotic ‎syndrome related to oxidative stress in ns.‎ through studies and reviews, the causes, pathophysiology, sources, and agents of ‎renal oxidative stress have been elucidated over several decades. we reviewed studies on ‎reactive oxygen species (ros) formation and their relationship with ‎hypoalbuminaemia nephrotic syndrome. the pathogenic pathways that lead to renal fibrosis, ‎mechanisms of oxidative stress production during renal disorders, and medications that ‎specifically target oxidative stress during tubulointerstitial fibrosis and glomerulosclerosis are ‎explained in this article.‎ a distinguishing feature of ns is increased excretion of albumin and other ‎serum proteins. therapies that target oxidative stress have the potential to treat renal fibrosis, ‎given the importance of oxidative stress in renal nephrotic syndrome. ‎