Insulin resistance is associated with and may be causal in essential h
ypertension, but the relation between insulin resistance and hypertens
ion arising de novo in pregnancy is unclear. Transient hypertension of
pregnancy (new-onset nonproteinuric hypertension of late pregnancy) i
s associated with a high risk of later essential hypertension and thus
may have similar pathophysiology. To assess the association between g
lucose intolerance and subsequent development of proteinuric and nonpr
oteinuric hypertension in pregnancy in women without underlying essent
ial hypertension or overt glucose intolerance, we performed a retrospe
ctive case-control study comparing glucose levels on routine screening
for gestational diabetes mellitus among women subsequently developing
hypertension. Women who developed hypertension in pregnancy (n=97) ha
d significantly higher glucose levels on 50-g oral glucose loading tes
t (P<.01) and a significantly higher frequency of abnormal glucose loa
ding tests (greater than or equal to 7.8 mmol/L) (P<.01) than women wh
o remained normotensive (n=77). Relative glucose intolerance was parti
cularly common in women who developed nonproteinuric hypertension. Wom
en who developed hypertension also had greater prepregnancy body mass
index (P less than or equal to.0001) and baseline systolic and diastol
ic blood pressures (P less than or equal to.0001 for both), although a
ll subjects were normotensive at baseline by study design. However, af
ter adjustment for these and other potential confounders, an abnormal
glucose loading test remained a significant predictor of development o
f hypertension (P<.05) and, specifically, nonproteinuric hypertension
in pregnancy (P<.01). Among a subgroup of women in whom insulin levels
were also measured (n=80), there was a nonsignificant trend toward hi
gher insulin levels in women developing hypertension. These results su
ggest that relative glucose intolerance is associated with an increase
d risk of new-onset hypertension in pregnancy, particularly the nonpro
teinuric type, and indirectly support the hypothesis that insulin resi
stance may play a role in the pathogenesis of this disorder.