S Kinra1, B Rath, B C Kabi. 1. Department of Public Health, South and West Devon Health Authority, Dartington, Devon TQ9 6JE, UK. Sanjay.Kinra@sw-devon-ha.swest.nhs.uk
Abstract
AIMS: To test the hypothesis that oxygen free radicals are mediators of excessive protein permeability in steroid responsive nephrotic syndrome. DESIGN: Case control study. PATIENTS: 20 children with steroid responsive nephrotic syndrome; controls: 20 children admitted for elective surgery. SETTING: 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.
AIMS: To test the hypothesis that oxygen free radicals are mediators of excessive protein permeability in steroid responsive nephrotic syndrome. DESIGN: Case control study. PATIENTS: 20 children with steroid responsive nephrotic syndrome; controls: 20 children admitted for elective surgery. SETTING: 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.
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