Thyroid hormone modulation of glucocorticoid-induced polycystic kidney disease.

N ormal growth and development of the mammahan kidney are partly regulated by hormones, and administration of glucocorticoid hormones (GC) at specific times during development causes polycystic kidney disease (PKD) in a number ofanimal species (1). In inbred mice, where metanephrogenesis continues until about the 20th postnatal day (2), the “timewindow” for cyst induction by exogenous glucocorticoids extends into the first few days oflife (3). Because hormonal manipulation, genetic variation, and environmental changes influence the incidence and severity of this GC-induced disease, it is consistent with a multifactorial threshold trait (1). In the early neonatal period of both human and musine development, there are significant changes in GC and thyroid hormone (TI-I) metabolism (4). There are many interrelationships between the effects of Th and GC, and the receptors of these hormones act through similar and sometimes contiguous hormone-responsive elements of target genes (5). We report evidence of an effect of Th on cystogenesis in this mouse model.