We studied 40 women in the third trimester of pregnancy to determine whether alterations in serum calcium levels or in urinary calcium excretion would distinguish patients with preeclampsia from normal pregnant women or women with other forms of gestational hypertension. Our population included 10 normal pregnant women, 5 pregnant women with transient hypertension, 6 with chronic hypertension, 7 with chronic hypertension and superimposed preeclampsia, and 12 with preeclampsia. The serum levels of ionized calcium, phosphate, and 1,25-dihydroxyvitamin D were not different among the various groups. In contrast, the mean (+/- SD) 24-hour urinary calcium excretion in the patients with preeclampsia or hypertension with superimposed preeclampsia was significantly lower (42 +/- 29 and 78 +/- 49 mg) than that in normal pregnant women (313 +/- 140 mg per 24 hours), women with transient hypertension (248 +/- 139 mg per 24 hours), or women with chronic hypertension (223 +/- 41 mg per 24 hours) (P less than 0.0001). The hypocalciuria in the women with preeclampsia was associated with a decreased fractional excretion of calcium. Although the mean creatinine clearance was reduced in the women with preeclampsia, the range of values overlapped with those in the other groups. In contrast, we observed little or no overlap with respect to calcium excretion. We conclude that preeclampsia is associated with hypocalciuria due to increased tubular reabsorption of calcium. Measurement of calcium excretion may be useful in distinguishing preeclampsia from other forms of gestational hypertension.
We examined renal tubular function in six patients with sickle cell hemoglobin. All had normal inulin and para-aminohippurate clearances and impaired urinary concentrating and acidifying abilities. After intravenous potassium chloride administration, maximum excretion of potassium (U,V) was significantly lower in sickle cell patients than in control subjects, and the percentage of potassium load excreted in 5 h was markedly reduced. Urinary potassium excretion after sodium sulfate infusion was also markedly reduced in sickle cell patients compared to control subjects. After 40 mg of oral furosemide, U,V was also diminished in sickle cell patients. Plasma aldosterone response to ACTH and intravenous potassium was similar to that of control subjects. Plasma renin activity increased normally after volume contraction. We conclude that sickle cell patients have a defect in their ability to excrete an acute potassium load that cannot be attributed to abnormal renin or aldosterone secretion. Overall potassium homeostasis is maintained by extrarenal mechanisms during acute potassium loading.
The hypothesis that aberrant maternal-fetal immunity might lead to the development of preeclampsia was examined using mixed lymphocyte culture reactions (MLC) as an in vitro analogue of maternal-fetal immunity. Maternal lymphocytes and serum from five normal pregnant women differed significantly from lymphocytes and serum from five preeclamptics. Maternal cells from normal pregnancy responded appropriately to unrelated control cells, but demonstrated selective hyporesponsiveness to fetal cells in the MLC. Serum from normal pregnancy suppressed MLCs when maternal cells were responder cells (RC) and maternal cells or fetal cells were stimulator cells (SC), and did not inhibit MLCs where maternal cells were RC and control cells were SC. Maternal lymphocytes and serum from preeclamptics did not demonstrate cellular hyporesponsiveness or humoral suppressor activity. Our findings support the notion that specific cellular hyporesponsiveness and humoral suppressor activity is responsible for normal pregnancy; absence of such adaptive immunity might lead to the development of preeclampsia.
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