AI Article Synopsis

  • There is evidence linking oxidative damage to kidney injury in patients with nephrotic syndrome (NS), suggesting a potential biomarker role for dynamic thiol/disulphide homeostasis (DTDH).
  • A study involving 39 NS patients and 40 healthy controls used an automated method to measure DTDH levels, finding significant differences during various phases of the disease.
  • Results indicated altered DTDH levels in NS patients, with shifts towards disulphide formation observed even during remission, highlighting a need for further understanding of oxidative stress mechanisms to inform new treatment strategies.

Article Abstract

Background: There is a growing body of evidence showing that there is an association between oxidative damage and kidney injury in patients with nephrotic syndrome (NS). Dynamic thiol/disulphide homeostasis (DTDH) is an important antioxidant system. The aim of this study was to determine if DTDH could be used as a biomarker of antioxidant status in pediatric NS patients using a novel automated method.

Methods: The study included 39 patients with NS and 40 healthy controls. The DTDH level was measured using a calorimetric and automated method developed by Erel and Neselioglu. In the NS group, DTDH was measured during first-attack episode, relapse, and remission.

Results: The native thiol, total thiol, and disulphide levels were significantly lower, the native thiol/total thiol ratio was significantly lower, and the disulphide/native thiol and disulphide/total thiol ratios were significantly higher in the NS patients during relapse and first-attack episode than during remission and in the controls. In addition, the native thiol and total thiol levels, and the native thiol/total thiol ratio were significantly lower, and the disulphide/native thiol and disulphide/total thiol ratios were significantly higher in the NS group during remission than those in the control group.

Conclusions: The present findings show that DTDH shifted toward disulphide formation in the NS patients, even during remission. A clearer understanding of the mechanism of this disruption to homeostasis in NS patients might lead to the development of novel therapeutic strategies.

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Source
http://dx.doi.org/10.1159/000496619DOI Listing

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