Hypocalciuria of preeclampsia is independent of parathyroid hormone level

Yair Frenkel, Gad Barkai, Shlomo Mashiach, Eran Dolev, Reuven Zimlichman, Mordechai Weiss*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Hypocalciuria is a feature of preeclampsia. The roles of parathyroid hormone (PTH) and vitamin D 1,25(OH)2D3 (calcitriol) in its pathogenesis have not yet been determined. Fourteen preeclamptic women were compared with 12 women with chronic hypertension and 11 normotensives, all in the third trimester. Preeclamptics had the lowest urinary calcium excretion rate (62.1 ± 32.8 mg/24 hours) compared with chronic hypertensive women (162.6 ± 97.8 mg/24 hours) and normotensive controls (225.6 = 146.9 mg/24 hours) (P < .05). Serum PTH was lowest in preeclamptics (9.8 ± 5.5 pg/mL), in contrast to the chronic hypertensives (18.5 ± 2.7 pg/mL) and normotensives (16.4 ± 3.2 pg/mL) (P < .005). Similarly, urinary cyclic adenosine monophosphate (cAMP) excretion was 2.9 ± 1.4 μmol/24 hours in the preeclamptics, 5.1 ± 1.7 μmol/24 hours in the chronic hypertensives, and 4.6 ± 1.3 μmol/24 hours in the normotensive group (P < .05). These data suggest that the mechanism of hypocalciuria in preeclampsia is independent of the PTH-calcitriol axis. Therefore, it is suggested that the hypocalciuria of preeclampsia is due to intrinsic renal tubular dysfunction.

Original languageEnglish
Pages (from-to)689-691
Number of pages3
JournalObstetrics and Gynecology
Issue number5
StatePublished - May 1991


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