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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 less than .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 less than .005). Similarly, urinary cyclic adenosine monophosphate (cAMP) excretion was 2.9 +/- 1.4 mumol/24 hours in the preeclamptics, 5.1 +/- 1.7 mumol/24 hours in the chronic hypertensives, and 4.6 +/- 1.3 mumol/24 hours in the normotensive group (P less than .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.
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PMID:Hypocalciuria of preeclampsia is independent of parathyroid hormone level. 184 25

A number of laboratory tests are available for the evaluation of the hypertensive gravida. These tests can be used to either predict and/or prognosticate between preeclampsia and other hypertensive disorders of pregnancy. These laboratory tests were evaluated based on published experience with special attention to its ability to facilitate identification of the patient with preeclampsia apart from other hypertensive disorders that co-exist with and occur as a complication of pregnancy. Hypocalciuria and increased cellular plasma fibronectin seem to be good tests to differentiate preeclampsia from chronic hypertension. The management of preeclampsia with its increased risk of perinatal morbidity and mortality renders this differentiation clinically very important. Hyperuricemia, proteinuria, increased serum beta-thromboglobulin concentration, abnormal red blood cell morphology with increased hemoglobin/hematocrit, and increased serum iron individually and collectively reflect the severity of preeclampsia. Platelets and total serum lactate dehydrogenase are the best tests to reflect the severity of HELLP syndrome. Circulating hCG and serum thromboglobulin seem to be the most promising future predictors for preeclampsia.
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PMID:The laboratory evaluation of hypertensive gravidas. 773 26

Hypocalciuria due to reversibly enhanced tubular calcium reabsorption in preeclampsia has been previously described. As the fetus is exposed in utero to the toxemic environment, its kidney function may be similarly affected. We therefore evaluated the amniotic fluid (AF) concentrations of Ca2+, Mg2+, Zn2+, and Na+ in relation to creatinine in 12 preeclamptic women, 9 pregnant women with chronic hypertension, and 12 control pregnant women. Our data reveal an increased AF Ca2+, Mg2+, and Zn2+ to creatinine ratio in preeclampsia 451 +/- 283; 164 +/- 94; 787 +/- 124 Eq/mol, respectively) as compared with chronic hypertension (256 +/- 141; 94 +/- 46; 504 +/- 124 Eq/mol, respectively), and normal controls (274 +/- 132; 83 +/- 19; 477 +/- 124 Eq/mol, respectively; p < 0.05). Na+ concentration did not vary significantly among the three groups. It is suggested that the higher AF divalent cation concentration in preeclampsia may be due to lower maternal urinary excretion thereby increasing the fetal divalent cation load.
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PMID:Increased amniotic fluid divalent cation concentration in preeclampsia. 856 80

Sixty five women were in the third trimester of pregnancy (29-40 weeks of gestation) submitted to the study including 35 with primary hypertension (the studied group) and 30 healthy (control group). The following parameters were measured in blood serum and urine from 24 hrs, collection: total Ca and Ca++, inorganic phosphorus (Pi) and magnesium. Generally accepted micromethods were used; Ca++ was measured using AVL type 9140 analyser. Women of the studied group presented mean blood pressure 164 +/- 14/106 +/- 9.7 mm Hg and did not have proteinuria and oedema. They presented decreased concentrations of total Ca (p < 0.004) and ionised Ca++ (p < 0.004), and an increase of Pi (p < 0.002) in blood serum. No differences in magnesium concentrations were found. Distinct decrease of calcium excretion in urine was found in hypertensive women (4.50 +/- 2.76 vs 6.60 +/- 3.4 mmol/24 hrs, p < 0.024). No alterations in phosphorus and magnesium urine excretion were observed in women with hypertension (women of both groups had the same volume of 24 urine). Our study concludes the main alterations in calcium-phosphorus-magnesium homeostasis in pregnant women with primary hypertension are the calcium homeostasis alterations. Phosphorus homeostasis is less affected while magnesium distribution does not change. Hypocalciuria might be related to impaired glomerular filtration in this pathology in pregnancy. Hypocalciuria and lowered serum concentrations of total Ca and ionised Ca++ might prove general deficiency of this element in pregnancy complicated by primary hypertension.
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PMID:[Calcium, phosphorus and magnesium in pregnant women with primary hypertension]. 929 44

The preeclampsia-eclampsia syndrome is a vasospastic disorder and probably has a placental origin. Once the hypertensive syndrome is established the uteroplacental blood flow is reduced as well as the intervillous blood flow. Since 18-24 weeks of gestation and before the symptoms of preeclampsia become overt, changes in placental flow velocity can be detected with Doppler technics. The placental theories for the etiology of preeclampsia are focused on the hypoxic effect in the trophoblastic tissue of second trimester. The placental ischemic changes are evident and seen in the uteroplacental bed. They are interrelated with the stages of trophoblastic invasion of the spiral arteries during the 14 and 20 weeks. When the trophoblastic invasion is over, the spiral arteries become a high resistance system. The defect observed in preeclampsia is the lack of invasion of the trophoblast to the maternal arteries. The diminished placental perfusion probably creates endothelial damage. This damage has several effects: decreased prostaglandin production, activated coagulation cascade, stimulated fibrin aggregation, and increased vascular permeability. The ideal laboratory test for preeclampsia shall predict the onset of this entity. Recent findings seem promising. The fibronectin concentration increases 2-3 wks. prior to the clinical manifestation of preeclampsia. Severe hypertension shows an abnormal decrease in fibronectin levels. Hypocalciuria has been described as an early predictor in the development of preeclampsia. Other agents undergoing extensive evaluation as predictors are: uric acid, b-thromboglobin, prolactin and atrial natriuretic peptide. Recently high levels of b-HCG (human corionic gonadotrophin) have been linked to a lack of trophoblastic invasion during the second trimester, therefore this is a potential marker for those patients that will eventually develop preeclampsia.
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PMID:[Observations on pe-eclampsia-eclampsia and the advances in the evolution of some laboratory tests]. 931 19

Hypocalciuria has been associated with preeclampsia (gestational hypertension with proteinuria or other maternal organ dysfunction) but not usually with pure gestational hypertension or normal pregnancy. We hypothesized that hypocalciuria would be a marker of emerging preeclampsia in women presenting with gestational hypertension who later developed preeclampsia. Eighty-one women with de novo hypertension in the second half of pregnancy (n = 81) were enrolled prospectively. At first assessment, calcium/creatinine ratio was determined in a spot urine. Patients were followed until delivery and were classified subsequently according to the occurrence of preeclampsia. Gestational hypertensive patients who became preeclamptic (n = 31) had lower urinary calcium/creatinine ratios at presentation (ratio = 0.07, interquartile range [IQR] = 0.04-0.11) than women who remained as gestational hypertensives (n = 50; ratio = 0.17, IQR = 0.08-0.21; P = .002). Intact plasma parathyroid hormone (PTH) concentrations were similar between groups. Using a receiver operator curve, the best threshold value for the development of preeclampsia was a calcium/creatinine ratio of 0.10, which yielded a sensitivity of only 68% and a specificity of 70%. A low calcium/creatinine ratio preceded the emergence of preeclampsia by 12 (7-24) (median [IQR]) days among a group of women with gestational hypertension. Though this implies primary or secondary disturbances of renal calcium handling even before preeclampsia is clinically apparent, this measurement does not have sufficient sensitivity to recommend its use as a screening test for the emergence of preeclampsia.
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PMID:Urinary calcium/creatinine ratio as a predictor of preeclampsia. 968 45