Objective
To assess the occurrence of chronic hypertension and renal disorder after gestations complicated by pregnancy induced hypertension or pre‐eclampsia and to define background factors and laboratory analyses at follow up examination which discriminate between women who remain normotensive and those who develop hypertension.
Setting
Swedish university hospital.
Subjects
Women with pregnancy induced hypertension (PIH) (n= 49), pre‐eclampsia (n= 45) or a normotensive pregnancy (n= 44) during 1986.
Design
Subjects were reviewed in 1993 with regard to chronic hypertension and renal disorder. Plasma concentrations of creatinine, urea, uric acid, calcium and albumin were measured, and urine was examined for the presence of microalbuminuria and erythrocyte excretion rate. Those with and without hypertension at follow up were compared with regard to the renal function tests and possible features in the history which might predict chronic hypertension.
Results
Women with a history of pregnancy induced hypertension or pre‐eclampsia had an increased risk, relative to controls, for hypertension at follow up (37% and 20%vs 2%; P < 0.001), microalbuminuria (14% and 20%vs 2%; P < 0.05) and demonstrated increased plasma levels of albumin corrected calcium (2.41 [SE 0.021 and 2.40 [0.01] vs 2.32 [0.01] mmol/l; P < 0.001). The only factors significantly associated with hypertension at follow up were the presence of microalbuminuria (P= 0.0008) and having had a delivery prior to the index pregnancy (P= 0.0017).
Conclusions
The risk for chronic hypertension seven years after a pregnancy complicated with pregnancy induced hypertension or pre‐eclampsia is considerably increased. The presence of hypertension at follow up is closely related to residual renal disorder.
Summary. Sympatho‐adrenal and cardiovascular reactivity was studied in patients with pregnancy‐induced hypertension (PIH) and healthy pregnant controls subjected to an isometric handgrip test and a cold pressor test both during and after the pregnancy. At rest, heart rate was higher in the PIH group than in the control group both during and after pregnancy. Forearm vascular resistance was not affected by PIH or by pregnancy per se. During pregnancy arterial plasma adrenaline levels were suppressed in the control group both when compared with the PIH group and postpartum values. Arterial noradrenaline levels were similar and normal in the two groups at both examinations. The iso‐metric exercise increased systolic and diastolic blood pressures, heart rate and noradrenaline and reduced vascular resistance similarly in the PIH and control groups on both occasions. Vasoconstrictor responses to the cold pressor test were reduced during prenancy but there were no differences between the groups on either occasion. Noradrenaline responses to the cold pressor test were not influenced by PIH or by pregnancy per se. During pregnancy adrenaline responses to the two tests tended to be reduced in the controls but not in PIH. Our results indicate enhanced adrenomedullary activity in PIH when compared with the suppressed activity in normal pregnancy. Cardiovascular reactivity to the tests was similar in the PIH and control groups. The normal arterial noradrenaline levels at rest and during provocation do not support the contention of a generalized increase in sympathetic nerve activity in PIH
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