Dynamic Thiol/Disulphide Homeostasis in Children with Nephrotic Syndrome

Fatma Yazılıtaş1, Fatma Zehra Oztek-Celebi2, Özcan Erel3

  • 1Department of Pediatric Nephrology, Saglik Bilimleri University, Dr. Sami Ulus Maternity and Child Health and Diseases Training and Research Hospital, Ankara, Turkey, fmeryemesra@yahoo.com.

Nephron
|February 7, 2019
PubMed

Insights

Dynamic thiol/disulphide homeostasis (DTDH) is disrupted in pediatric nephrotic syndrome (NS) patients, even during remission. This indicates DTDH may serve as a biomarker for antioxidant status in NS, potentially guiding new therapies.

Area of Science:

  • Biochemistry
  • Pediatric Nephrology
  • Oxidative Stress Research

Background:

  • Oxidative damage is linked to kidney injury in nephrotic syndrome (NS).
  • Dynamic thiol/disulphide homeostasis (DTDH) is a key antioxidant system.
  • The role of DTDH as a biomarker in pediatric NS requires further investigation.

Purpose of the Study:

  • To evaluate DTDH as a biomarker of antioxidant status in pediatric NS patients.
  • To utilize a novel automated method for DTDH measurement.
  • To assess DTDH levels during different stages of NS (first attack, relapse, remission).

Main Methods:

  • Inclusion of 39 pediatric NS patients and 40 healthy controls.
  • Measurement of DTDH using a calorimetric and automated method.
  • Analysis of DTDH in NS patients during first attack, relapse, and remission.

Main Results:

  • NS patients exhibited significantly altered thiol/disulphide levels compared to controls.
  • DTDH showed a shift towards disulphide formation in NS patients during relapse and first attack.
  • Even in remission, NS patients displayed a DTDH imbalance compared to healthy controls.

Conclusions:

  • DTDH is significantly disrupted in pediatric NS patients, indicating a pro-oxidative state.
  • The findings suggest DTDH can serve as a potential biomarker for antioxidant status in NS.
  • Further research into the mechanisms of DTDH disruption may inform novel therapeutic strategies for NS.
Abstract

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