PRENATAL DEXAMETHASONE CAUSES OLIGONEPHRONIA, SODIUM RETENTION, AND HIGHER BLOOD-PRESSURE IN THE OFFSPRING

Recent reports have shown that low birth weight infants have a higher incidence of adult hypertension. These observations have stimulated a number of studies designed to evaluate the mechanisms of this phenomen on. In this study, fetal growth retardation was induced by treating pr egnant rats with dexamethasone. After birth, pups whose mothers were t reated with dexamethasone had a lower body and kidney weight and a low er number of glomeruli than control pups. Immunohistochemistry on trea ted kidneys demonstrated a marked reduction in the number of cells und ergoing mitosis in the cortical nephrogenic zone. In the treated group , body and kidney weight normalized by 60 d of age, but blood pressure was significantly higher compared with controls (130 +/- 4 versus 107 +/- 1 mm Hg). In addition, GFR was significantly lower, albuminuria w as higher, urinary sodium excretion rate and fractional sodium excreti on were lower, and sodium tissue content was higher. In contrast, when pregnant rats were treated with a natural glucocorticoid (hydrocortis one) which is metabolized by the placenta, fetal development and adult blood pressure were normal. In conclusion, we found that high levels of maternal glucocorticoids impair renal development and lead to arter ial hypertension in offspring. Even though renal mass eventually norma lizes, glomerular damage as well as sodium retention occur and these f actors may contribute to the development of hypertension.