Oxidative stress in the progression of Chronic Kidney Diseases in children

Abstract

Current studies show that the increase in the incidence of Chronic Kidney Disease cannot be fully explained only by risk factors well elucidated in the specialty literature, as knowing that oxidative stress is prevalent in Chronic Kidney Disease patients and is considered to be an important pathogenetic mechanism. Reactive oxygen species, which appear in excess as a result of ischemic, toxic or immune mediator changes, can negatively influence various pathological processes in renal pathology. These processes mainly refer to the pathogenesis of Chronic Kidney Disease or acute kidney injury. There are at least two pathophysiological mechanisms by which oxidative stress is formed in renal pathology, and then their damaging effects can cause, maintain or aggravate the cause of the condition. Following the initiation of inflammatory processes, the progression of renal damage is accelerated, with the eventual damage to all nephron structures as well as the interstitial space. The main sources of reactive oxygen species are mitochondria, but other cellular organelles may also be involved. Oxidant radicals produce oxidation of proteins, lipids, modification of nucleic acids with destruction of cell membranes, induction of apoptosis and lysis of kidney tissue. It is shown that free radicals are normally annihilated by superoxide dismutase – the antioxidant enzyme. There are several biomarkers that can be evaluated to detect oxidative stress and antioxidant status in patients with chronic kidney disease. Their determination in the context of a complex examination represents an informational support in the elucidation of pathogenetic mechanisms with the implementation of non-invasive early diagnosis methods. We reviewed the Chronic Kidney Disease literature to see if the guidelines and data are reliable enough to justify a particular approach.