Role of oxidant-antioxidant enzymes in managing the cardiovascular risks in nephrotic syndrome patients

Increased reactive oxygen species (ROS) in nephrotic syndrome (NS) are involved in the oxidation of membrane proteins, lipoproteins and several receptor molecules ultimately leading to their functional deficit. It is involved in the pathogenesis of dyslipidemia in NS and also increases the oxidation of LDL (oxLDL), which is an important risk factor in thrombus generation and atherosclerosis. Myeloperoxidase (MPO) is an early predictor of myocardial infarction and adverse cardiac events in patients with chest pain. MPO can also foresee the recurrent acute coronary syndrome (ACS) and myocardial infarction in patients. ‘MPO oxidized LDL’ also induces ROS production, lipid accumulation and reduces the antioxidant response in macrophages, however in an augmented way by using different pathways and might be more atherogenic. Paraoxonase 1 (PON1) prevents the oxidative modification of serum lipoproteins, which is one of the crucial steps in the initiation of atherogenesis. PON1 also contributes to the anti-atherogenic effect of HDL-c. Adult NS patients have increased lipid hydroxide levels and significantly decreased PON1 activity and total sulfhydryl levels when compared to healthy controls. While the increased risk of cardiovascular disease in NS patients is well documented, the exact etiology still remains controversial. This prevents the development of a specific treatment modality for the same. MPO as well as PON1 were found as important markers for the management of cardiovascular risk in NS patients. Estimation of these enzymes can therefore be performed in routine clinical practice as prognostic markers, owing to its ease of estimation and cost effectiveness.