RU38486 prolongs survival in murine congenital polycystic kidney disease.
The cpk/cpk mutant mouse develops a lethal infantile polycystic kidney disease that is associated with disregulation of post natal glucocorticoid production. To establish if the observed endocrine abnormality is involved in the pathophysiology of polycystic kidney disease, blockade of glucocorticoid action during the immediate post-natal period was attempted. The steroid antagonist, RU38486, when administered from day 3 to day 12 of post-natal life, prolonged survival in affected animals. This finding supports a role for steroid hormones in the pathogenesis of this form of polycystic kidney disease.
Ogborn
M R
MR
Department of Pediatrics, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada.
Crocker
J F
JF
McCarthy
S C
SC
D000818:Animals; D004963:Estrenes / Q000494:pharmacology*; D005938:Glucocorticoids / Q000037:antagonists & inhibitors*; D051379:Mice; D015735:Mifepristone; D007690:Polycystic Kidney Diseases / Q000209:etiology*
D004963:Estrenes; D005938:Glucocorticoids; D015735:Mifepristone