Abstract
Childhood nephrotic syndrome, in which steroid-dependence occurs concurrently with steroid-resistance, requires aggressive therapy to prevent relapse. Predictive biomarkers that can be used to stratify treatment are urgently needed. Here we report that reciprocal regulation of the glucocorticoid metabolizing enzymes, 11β-hydroxysteroid dehydrogenase types 1 and 2, is associated with steroid-responsiveness and disease remission in childhood nephrotic syndrome, potentially providing a marker to identify patients in which aggressive therapy is required.
Copyright © 2016 by the American Academy of Pediatrics.
MeSH terms
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11-beta-Hydroxysteroid Dehydrogenase Type 1 / blood*
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11-beta-Hydroxysteroid Dehydrogenase Type 2 / blood*
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Adolescent
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Anti-Inflammatory Agents / therapeutic use*
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Biomarkers / blood
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Child
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Child, Preschool
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Dexamethasone / therapeutic use
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Drug Administration Schedule
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Drug Resistance*
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Drug Tolerance*
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Female
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Humans
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Induction Chemotherapy
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Maintenance Chemotherapy
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Male
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Nephrotic Syndrome / blood
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Nephrotic Syndrome / diagnosis
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Nephrotic Syndrome / drug therapy*
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Nephrotic Syndrome / enzymology
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Prednisolone / therapeutic use*
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Receptors, Glucocorticoid / blood
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Recurrence
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Treatment Outcome
Substances
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Anti-Inflammatory Agents
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Biomarkers
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NR3C1 protein, human
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Receptors, Glucocorticoid
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Dexamethasone
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Prednisolone
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11-beta-Hydroxysteroid Dehydrogenase Type 1
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11-beta-Hydroxysteroid Dehydrogenase Type 2
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HSD11B1 protein, human
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HSD11B2 protein, human