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Related Experiment Videos

Glucocorticoid teratogenesis in the developing nephron.

J F Crocker1, M R Ogborn

  • 1Department of Pediatrics, Dalhousie University, Halifax, Nova Scotia, Canada.

Teratology
|June 1, 1991
PubMed
Summary
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Fetal exposure to glucocorticoids can induce polycystic kidney disease (PKD) in mice. This occurs during critical developmental periods, particularly after injections on gestational days 12 and 17.

Area of Science:

  • Developmental biology
  • Toxicology
  • Nephrology

Background:

  • Neonatal glucocorticoid exposure is a known inducer of polycystic kidney disease (PKD).
  • Limited data exist regarding the effects of fetal glucocorticoid exposure on kidney development and PKD induction.

Purpose of the Study:

  • To investigate the potential of in utero glucocorticoid exposure to induce polycystic kidney disease (PKD).
  • To identify critical developmental windows for glucocorticoid-induced PKD during gestation.

Main Methods:

  • Pregnant Swiss Webster mice received daily subcutaneous injections of hydrocortisone acetate (250 mg/kg) from day 1 to 19 of gestation.
  • Control groups received saline injections.
  • Offspring kidneys (n=1,522) underwent histologic analysis to assess for polycystic kidney disease.

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Main Results:

  • No polycystic kidneys were observed in the control group or offspring exposed before gestational day 11.
  • A bimodal distribution of cystic kidney disease was observed in offspring exposed on later days.
  • Highest prevalence of PKD occurred following injections on day 12 (50.8%) and day 17 (34.3%) of gestation.

Conclusions:

  • Glucocorticoid administration during specific gestational periods can induce polycystic kidney disease (PKD) in utero.
  • Gestational days 12 and 17 represent critical windows for glucocorticoid-induced metanephric development abnormalities leading to PKD.