The influence of dexamethasone on diuresis in preterm infants has not been
well studied. We examined 15 preterm infants at risk for chronic lung disea
se with gestational ages ranging from 26 to 29 wk (median 27.6 wk) and birt
hweights ranging from 700 to 1485 g (median 965 g). Urine output, blood glu
cose, serum urea, serum creatinine, serum sodium and serum potassium, as we
ll as systolic, diastolic and mean arterial pressure were measured on the d
ay before, and on 4 consecutive days after starting treatment with dexameth
asone (0.25 mg kg(-1) i.v., twice daily). We found an increase of diuresis
of 30 mi kg(-1) d(-1), 48-96 h after starting dexamethasone treatment. This
coincided with a gradual but significant increase of serum urea levels and
arterial pressure. During the study period, fluid and protein intake remai
ned constant. Blood glucose and serum creatinine levels did not change. Our
findings suggest that the increased urine output following dexamethasone t
reatment might be caused by two factors: (1) pressure diuresis induced by t
he increase of arterial pressure and (2) an increase of the osmolar load to
the kidney due to an increase of serum urea.
Conclusions: This study demonstrates that a significant increase of diuresi
s occurs in preterm infants, 48-96 h after starting dexamethasone. A carefu
l monitoring of fluid balance during the first days of dexamethasone treatm
ent is recommended.