Oxidative stress in children with nephrotic syndrome

Abstract

Sir,The letter to the editor by Kaneko and colleagues reportingchanges in urinary 8-hydroxydeoxyguanosine (8-OH-DG)in idiopathic nephrotic syndrome adds further importantinformation to the role played by oxidative stress in acuteglomerular disease [1].Free radicals are extremely reactive compounds thatinteract with lipids, proteins, and nucleic acids. The kidneyphysiologically generates a small amount of reactiveoxygen species (ROS) as part of oxidative metabolism,which is well tolerated. If generated in larger amountslocally, ROS may conceivably cause or contribute to thedamage of glomerular structures, leading to altered glomer-ular permselectivity.Whereastheincreasedplasmalevelsofmalonyldialdehydeand nitrite observed by us and others in acute nephroticsyndrome signal increased lipid and protein peroxidation[2, 3], the increased urinary excretion of 8-OH-DG asobserved by Kaneko et al. reflects the interaction of ROSwith cellular DNA [1]. Hence, their finding nicelycomplements the concept of an imbalance of ROSinduction and impaired antioxidant mechanisms in acutenephrotic syndrome [2, 3]. With respect to the specificityof this potential pathophysiological mechanism, it is ofnote that no increase in 8-OH-DG occurred in threepatients with acute poststreptococcal glomerulonephritis.If this preliminary observation is confirmed, it would lendsupport to a specific role of oxidative stress in idiopathicnephrotic syndrome.References