Oxidative stress mechanisms as potential therapeutic targets in chronic kidney disease

Abstract

Chronic kidney disease (CKD) is a gradual loss of kidney function over time, leading to the development of kidney failure. CKD is a consequence of common civilization diseases, such as arterial hypertension and diabetes, as well as primary kid- ney and urinary tract diseases of various aetiologies. The pathogenesis of CKD is complex, and the ongoing inflammation and increased oxidative stress (OS) in kidney tissues also play a significant role in the CKD pathophysiological description. Hence, attempts are being made to pharmacologically modify these important pathophysiological pathways. This article presents a brief overview of the aetiopathogenesis of OS in the course of CKD and briefly lists the research on the novel com- pounds with expected OS-alleviating activity in CKD based on their interference with selected pathophysiological pathways (xanthine oxidase inhibitors, nicotinamide adenine dinucleotide phosphate oxidase inhibitors, protein kinase C inhibitors, transforming growth factor β inhibitors, or activators of nuclear factor erythroid 2-related factor 2).