Abstract

Aim:The purpose of this study was to investigate the change of the plasma oxidative stress level in children with IgA nephropathy (IgAN) and analyze its relativity to the clinical and pathological classification. To discuss the early effects of angiotensin-converting enzyme inhibitors (ACEIs) on the plasma oxidative stress level in children with IgA nephropathy.Methods:Thirty-eight children with IgAN were divided into groups according to their clinical features, pathologic grades, and treatments. Twenty healthy children were included in the control group.Results:The plasma level of advanced oxidation protein products (AOPPs), malonaldehyde (MDA), and superoxide dismutase (SOD) were detected. The plasma level of oxidative stress was significantly increased in the IgAN group, including a higher plasma level of AOPP and MDA and a lower plasma level of SOD. After treatment, the plasma level of oxidative stress was significantly decreased in the ACEI group.Conclusions:The children with IgAN had an increase in the plasma level of oxidative stress, expressed as an increased plasma level of AOPP and MDA and a decreased plasma level of SOD. Oxidative stress was associated with the progression of IgAN in children. Early treatment with ACEI therapy can significantly reduce the plasma level of oxidative stress in children with IgAN.

Highlights

  • IgA nephropathy (IgAN) is the most common primary glomerular disease in children, and its pathogenesis has not been fully elucidated

  • This study investigates the plasma oxidative stress level in children with IgAN, compares the relationship to clinical pathology, and presents the influence of Angiotensinconverting enzyme inhibitors (ACEIs) on oxidative stress by testing advanced oxidation protein products (AOPPs), malonaldehyde (MDA) and superoxide dismutase (SOD) levels

  • There was a positive correlation between oxidative stress indicator levels and serum cystatin C (Cys-C) level and oxidative stress level and 24-hour urine protein level

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Summary

Introduction

IgA nephropathy (IgAN) is the most common primary glomerular disease in children, and its pathogenesis has not been fully elucidated. A study with a 20-year follow-up shows that 30% of patients with childhood IgAN developed end-stage renal disease (ESRD).[1,2] Angiotensinconverting enzyme inhibitors (ACEIs) are one of the recognized medications for delaying the progression of nephropathy through a mechanism that is not related to blood pressure effects.[3,4,5,6,7,8] Over a decade ago, it was observed that angiotensin II (Ang II) can activate NADPH oxidase that mediates reactive oxygen species (ROS) production.[9,10] It has been clinically demonstrated that the immunoreactivities of intrarenal heme oxygenase-1 (HO1) and 4-hydroxy-2-nonenal (4-HNE) (markers of ROS) and those of intrarenal angiotensinogen (AGT) and angiotensin II (Ang II) (markers of the renin angiotensin system (RAS)) in IgA nephropathy patients were significantly increased compared to those of control subjects.

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