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. ‎