Abstract
Objective:Growing evidence shows that oxidative stress plays an important role in the development and progression of nephrotic syndrome (NS). In this study, we aimed to examine serum IMA levels as an indicator of oxidative stress in children with steroid-sensitive NS (SSNS) in remission and relapse.Methods:This cross-sectional study was carried out at the Pediatric Nephrology Unit of Sanliurfa Training and Research Hospital, Sanliurfa, Turkey, from April 2019 to December 2019. In this study Serum IMA and albumin levels were determined in 70 children with SSNS and 45 healthy controls. Among the children with SSNS, 50 were in remission and 20 were in relapse. Then, adjusted IMA levels were calculated from the IMA/albumin ratio.Results:IMA and adjusted IMA levels significantly increased and albumin significantly decreased in children with SSNS in relapse and remission compared with those of the healthy controls. Moreover, these alterations were more prominent in the relapse group than in the remission group. IMA was inversely correlated with albumin in children with SSNS (r= −0.881, p= <0.001).Conclusions:Our findings demonstrated that elevated IMA and adjusted IMA levels observed in patients with SSNS were associated with increased oxidative stress and could indirectly reflect the degree of oxidative damage in glomerular structures.
Highlights
Nephrotic syndrome (NS) is a kidney disease with an estimated incidence of 1.15–16.9 per 100,000 children
ischemia-modified albumin (IMA) and adjusted-IMA levels were significantly higher and albumin levels were significantly lower in the sensitive NS (SSNS)-relapse group than in the SRNS-remission and control
These results reveal that higher IMA levels observed in NS patients are associated with increased oxidative stress and may indirectly reflect oxidative protein damage
Summary
Nephrotic syndrome (NS) is a kidney disease with an estimated incidence of 1.15–16.9 per 100,000 children. The main manifestations of this disease include severe proteinuria, hypoalbuminemia, edema, and lipid abnormalities. The pathogenesis of NS is not fully known, but evidence suggests that it may be related to immunological mechanisms, podocyterelated factors, and genetic variants.[1] Some studies support the hypothesis that oxidative stress plays a crucial role in the development and progression of various kidney diseases, including NS.[2,3,4] Oxidative stress, which results from the imbalance between the production of reactive oxygen species (ROS) and their elimination by antioxidants, can cause undesirable effects on. Studies have shown a significant correlation between levels of several oxidative stress parameters and proteinuria in patients with NS.[7,8]
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