Calcium Metabolism, Plasma Parathyroid Hormone, and Calcitriol in Transient Hypertension of Pregnancy

In order to know if abnormalities of calcium metabolism may be involved in the pathophysiology of pregnancy-induced hypertension (PIH), as it has been incriminated in essential hypertension, we measured plasma and urinary calcium and phosphate as well as plasma PTH and free calcitriol index (ratio of total calcitriol on the D binding protein) in normotensive pregnant women (n = 25), in women with PIH after the same duration of amenorrhea ( > 28 wk, η = 21: preeclampsia and 20 transient hypertensions), and in age-matched nonpregnant women (n = 15). The severity of PIH was mild since blood uric acid was not increased and plasma volume, measured with the Evans blue technique, was found only moderately decreased (—10.5 ± 3.1% of normal value). The results show that normotensive pregnant women showed the expected increase of the vitamin D parameters in comparison to nonpregnant controls. Hypertensive pregnant women were not different from the normotensive ones regarding plasma corrected calcium and phosphate and urinary excretion of calcium and phosphate, but had higher plasma PTH (13 ± 1 ν 8.8 ± 1.6 pg/mL ) and lower total and free calcitriol index (86 ± 7 ν 110 ± 6 pg/mL and 1.72 ± 0.10 ν 2.25 ± 0.13 Χ 1 0 " 5 ) . Correlative studies showed PIH having a negative correlation between blood pressure and plasma corrected calcium (r = —0.43, P< .05), which is in agreement with epidemiological studies of essential hypertension. In conclusion, disturbances of calcium regulating hormones do exist in transient forms of pregnancy-induced hypertension. In contrast to their increase in essential hypertension, plasma calcitriol levels are not so high in transient hypertension of pregnancy as compared to normotensive pregnancy, as it has been already shown in preeclampsia. All the above data taken together suggest that in both forms of pregnancy- induced hypertension, there is a primary defect of calcitriol synthesis in contrast to essential hypertension. Am J Hypertens 1993;6:522–527