Reciprocal Regulation of 11β-HSDs May Predict Steroid Sensitivity in Childhood Nephrotic Syndrome

Pediatrics. 2016 Sep;138(3):e20154011. doi: 10.1542/peds.2015-4011. Epub 2016 Aug 9.

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.

MeSH terms

  • 11-beta-Hydroxysteroid Dehydrogenase Type 1 / blood*
  • 11-beta-Hydroxysteroid Dehydrogenase Type 2 / blood*
  • Adolescent
  • Anti-Inflammatory Agents / therapeutic use*
  • Biomarkers / blood
  • Child
  • Child, Preschool
  • Dexamethasone / therapeutic use
  • Drug Administration Schedule
  • Drug Resistance*
  • Drug Tolerance*
  • Female
  • Humans
  • Induction Chemotherapy
  • Maintenance Chemotherapy
  • Male
  • Nephrotic Syndrome / blood
  • Nephrotic Syndrome / diagnosis
  • Nephrotic Syndrome / drug therapy*
  • Nephrotic Syndrome / enzymology
  • Prednisolone / therapeutic use*
  • Receptors, Glucocorticoid / blood
  • Recurrence
  • Treatment Outcome

Substances

  • Anti-Inflammatory Agents
  • Biomarkers
  • NR3C1 protein, human
  • Receptors, Glucocorticoid
  • Dexamethasone
  • Prednisolone
  • 11-beta-Hydroxysteroid Dehydrogenase Type 1
  • 11-beta-Hydroxysteroid Dehydrogenase Type 2
  • HSD11B1 protein, human
  • HSD11B2 protein, human