title: Indirect quantification of lipid peroxidation in steroid responsive nephrotic syndrome.
abstract: OBJECTIVE
  To test the hypothesis that oxygen free radicals are mediators of excessive protein permeability in steroid responsive nephrotic syndrome.
  
  
  METHODS
  Case control study.
  
  
  METHODS
  
  
  
  METHODS
  20 children with steroid responsive nephrotic syndrome; controls: 20 children admitted for elective surgery.
  
  
  METHODS
  The paediatric and biochemistry departments of the Maulana Azad Medical College, New Delhi, India.
  
  
  METHODS
  Blood samples were taken twice from children with nephrotic syndrome (on admission and on urinary remission) and once from controls. Biochemical assays were carried out on these blood samples to quantify the indirect markers of free radical injury in the body, namely: vitamin E, reduced glutathione (GSH), glucose-6-phosphate dehydrogenase (G6PD), malonyldialdehyde (MDA), and membrane cholesterol in erythrocytes.
  
  
  RESULTS
  There was some evidence supportive of oxidative injury in the children with nephrotic syndrome in the form of greatly reduced concentrations of antioxidants vitamin E (155.4 microg/100 ml in controls, 86.4 microg/100 ml in patients) and G6PD (364 mU/ml in controls, 205.1 mU/ml in patients). However, concentrations of the oxidation byproduct MDA were raised only in the remission phase of the disease (0.984 nmol/ml in controls, 1.158 nmol/ml in cases), whereas those of GSH were unaltered.
  
  
  CONCLUSIONS
  Changes in the concentrations of MDA, G6PD, and vitamin E are consistent with increased amounts of oxidation in steroid responsive nephrotic syndrome. Further research is needed to explain whether these changes are a cause or consequence of the disease.
authors.affiliation: Department of Public Health, South and West Devon Health Authority, Dartington, Devon TQ9 6JE, UK. Sanjay.Kinra@sw-devon-ha.swest.nhs.uk
authors.forename: S
authors.initials: S
authors.lastname: Kinra
authors.forename: B
authors.initials: B
authors.lastname: Rath
authors.forename: B C
authors.initials: BC
authors.lastname: Kabi
mesh_terms: D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D002784:Cholesterol / Q000097:blood / Q000378:metabolism; D005260:Female; D005609:Free Radicals / Q000378:metabolism; D005954:Glucosephosphate Dehydrogenase / Q000097:blood / Q000378:metabolism; D006801:Humans; D015227:Lipid Peroxidation / Q000502:physiology*; D008297:Male; D008315:Malondialdehyde / Q000097:blood / Q000378:metabolism; D009404:Nephrotic Syndrome / Q000188:drug therapy / Q000378:metabolism*; D011239:Prednisolone / Q000627:therapeutic use; D011507:Proteinuria / Q000209:etiology; D014810:Vitamin E / Q000097:blood / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D005609:Free Radicals; D014810:Vitamin E; D008315:Malondialdehyde; D002784:Cholesterol; D011239:Prednisolone; D005954:Glucosephosphate Dehydrogenase