HLA-DRB types in pre-eclampsia and eclampsia.
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Biomedical subjects
Publications and source records attributed to E D Gallery.
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The use of transluminal percutaneous renal angioplasty for severe hypertension in the second trimester of pregnancy has not previously been reported. We describe its use in a 19-year-old female. The procedure resulted in a significant improvement in blood pressure control and allowed the pregnancy to proceed to term, resulting in the delivery of a normal female baby on the 90th percentile for weight. No morbidity to mother or fetus was observed as a result of diagnostic or therapeutic procedures. We conclude that pregnancy should not preclude making the diagnosis of renovascular hypertension as angioplasty may be a useful therapeutic option.
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To aid investigation into the clinical problem of hematuria, assessment of abnormalities in the shape of red cells in the urine (dysmorphism) is gaining popularity in nephrology. However, there is uncertainty in the literature regarding both the number of red blood cells (RBC) in normal urine, as well as the quantification of dysmorphism. We have shown that in normal urine (N = 27) the number of RBC is less than 2,000/ml as assessed by scanning electron microscopy of filtered urine specimens from normal volunteers without known renal disease, which compared to less than 1,000/ml by centrifugation and phase contrast microscopy of the same specimen. To determine whether dysmorphism of urinary red blood cells was a significant predictor of glomerular disease we compared the number of dysmorphic cells in the urine of patients with biopsy proven glomerulonephritis (GN), before and immediately after renal biopsy. We also compared the number of dysmorphic cells in patients with glomerulonephritis to those with lower urinary tract bleeding. Renal biopsy caused significant dysmorphic hematuria, indicating that dysmorphism suggests renal rather than glomerular bleeding. Although patients with GN had significantly more dysmorphic urinary RBC when compared to those with lower tract urinary bleeding, the overlap was such that one could only be confident of renal hematuria if they accounted for greater than 75% of the total number of RBC. Non renal hematuria is present if number of dysmorphic cells is less than 17% of total RBC. Thus dysmorphism of urinary RBC is a useful diagnostic tool, but only if strict criteria established for each laboratory are adhered to.
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One hundred fifty-eight intravenous saline solution infusions (3 mmol Na per kilogram body weight) were performed in (1) normal primigravid women during the second and third trimesters and post partum, after 1 week of either a high, low, or ad libitum salt intake; (2) normotensive primigravid women during midpregnancy who later developed pregnancy-induced hypertension, and (3) seven proteinuric and seven nonproteinuric primigravid women with ad libitum salt intake who had established pregnancy-induced hypertension. Sodium excretion did not differ significantly between pregnancy and after pregnancy despite marked differences in plasma renin activity, aldosterone concentration, volume, and glomerular filtration rate. Sodium excretion after saline solution loading varied according to prestudy sodium intake and was reduced between the second and third trimesters, independent of dietary salt intake. Those destined to develop pregnancy-induced hypertension had sodium excretion similar to that of continuously normotensive subjects during the second trimester, but those with established proteinuric pregnancy-induced hypertension had the lowest plasma volume, plasma aldosterone concentration, and plasma renin activity and retained sodium to the same degree as salt-deplete women with normotension. These results demonstrate that the balance of sodium regulatory factors is similar between pregnancy and post partum, that prestudy salt intake and stage of gestation can alter the natriuretic response to saline solution loading, and that normal pregnant women retain more administered sodium in late pregnancy than in midpregnancy despite further increases in plasma volume and no alterations to blood pressure or glomerular filtration rate. Those with established proteinuric pregnancy-induced hypertension retain sodium avidly without stimulation of plasma renin activity or plasma aldosterone concentration, findings not apparent during midpregnancy in those who later developed this disorder.
1. Active electrolyte transport was examined in erythrocytes from women in the second and third trimesters of pregnancy and post partum, and compared with that in ovulating women. 2. There was a significant reduction in intracellular sodium ([Na]i) and increase in intracellular potassium ([K]i) in pregnancy with a return towards normal values in the post-partum period. 3. Maximum specific ouabain binding [number of Na+,K+-adenosine triphosphatase (Na+, K+-ATPase) units] was increased by 70% in pregnancy and returned slowly towards normal values post partum. 4. Na+,K+-ATPase activity as determined by ouabain-sensitive 86Rb influx in artificial media was also increased in pregnancy by 13%. It returned towards normal post partum. 5. The increases in Na+,K+-ATPase in pregnancy were not closely related to the concomitant increases in aldosterone or cholesterol nor to reticulocytosis and were not affected by 7 days of high (greater than 250 mmol/day) or low (less than 50 mmol/day) sodium intake.
To examine the short-term regulation of sodium excretion, plasma volume, and the renin-aldosterone system in pregnancy, women in their first pregnancy received either a high-salt (HS) (250 mmol/day) or a low-salt (LS) (20 mmol/day) diet for 7 days during the second and third trimester and after delivery (total 213 studies). Twenty women, studied while normotensive during mid-pregnancy, developed pregnancy-induced hypertension (PIH) in the third trimester. There was slightly greater difficulty adapting to sodium depletion (LS diet) during normal pregnancy compared with postpartum. The final mean values for sodium excretion were 27 (SE 2), 28 (SE 3) and 14 (SE 4) mmol/day in the second and third trimester and postpartum respectively. Sodium excretion with the HS diet was similar at all stages and plasma volumes were maintained as effectively during pregnancy as after delivery following both diets. Plasma renin activity (PRA) and aldosterone concentration rose and fell significantly following the LS and HS diets but the sensitivity of renin response to changes in salt intake was blunted during normal pregnancy. Women who later developed PIH, when studied whilst normotensive, failed to stimulate plasma aldosterone after salt depletion in their second trimester and did not exhibit the 'sodium-independent' component of PRA seen in continuously normotensive subjects at this stage.
We assessed the relationship between maternal hypertension during pregnancy and the incidence of respiratory distress syndrome (RDS) in 263 infants born at 32 weeks' gestation or less. Two-hundred and twenty-three mothers were normotensive and 40 were hypertensive. RDS occurred significantly more commonly in infants of hypertensive mothers than in controls (60% vs 33%; p = 0.001). The association between maternal hypertension and an increased rate of RDS remained after adjustment for differences between groups with respect to gestational age, mode of delivery, administration of antenatal steroids and other complications of pregnancy, except for delivery in the absence of labour. The increased rate of RDS related to the severity of hypertension but did not relate to the duration of hypertension or to maternal treatment with beta-blockers. In those infants who developed RDS there was no significant difference in the severity of the illness between the hypertensive group and the controls.
C3 allotyping has been performed on 424 Australian women, 203 with normotensive pregnancies, 161 with hypertensive noneclamptic pregnancies and 60 eclamptic women. The frequency of women heterozygous for 'rare' C3 alleles was 1% in the normotensive women and 3.7% in the hypertensive group. Three out of 25 (12%) of the women with proteinuric hypertension in pregnancy carried 'rare' C3 alleles. This suggested the hypothesis that pre-eclampsia/eclampsia is associated with a higher frequency of rare alleles. The sample of 60 eclamptic women collected to test the hypothesis had no rare alleles, refuting the hypothesis. The frequency of the common (C3F, C3S) alleles did not differ significantly between the three groups. We conclude that there is no evidence for any association between susceptibility to eclampsia and allotypes of the C3 complement component.
Many physiological variables known or thought to affect erythrocyte Na+,K+-cotransport are altered in pregnancy. The interrelationships of Na+,K+-cotransport and pregnancy were therefore examined. Values were elevated by more than 30% in both second and third trimesters with a return towards non-pregnant levels in the postpartum period. Although pregnancy was also associated with elevated plasma cholesterol, renin activity and aldosterone, there was no significant relationship within the pregnant group between Na+,K+-cotransport and any of these factors. No change could be demonstrated in Na+,K+-cotransport values after 7 days of either high (greater than 250 mmol/day) or low (less than 50 mmol/day) sodium intake and values for those who developed pregnancy-associated hypertension (PAH, pre-eclampsia) were not significantly different from those in continuously normotensive women in either the second or the third trimesters of pregnancy.
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The relationship between plasma osmolality (Posm) and plasma arginine vasopressin (Pavp) was determined in: (1) 62 normal primigravidas (P) at various stages of gestation and 35 nonpregnant, healthy volunteers (NP) under conditions of normal hydration or water deprivation, and (2) a separate group of 29 normotensive primigravidas during both the second and third trimesters under normal hydration. Pavp was similar in the P and NP groups, and Posm and Pavp were correlated significantly in both groups, but the osmotic threshold was lowered by 11 mosm/kg in primigravidas. In the prospective study, Pavp and Posm were correlated significantly at both stages. Pavp rose between trimesters, as did plasma volume and plasma renin activity, but urine volume and osmolality and Posm did not change significantly. These data confirm that resetting of the osmostat is operative in primigravid pregnancy and extend these observations by demonstrating that this phenomenon is established at least as early as mid-pregnancy. Furthermore, the osmoregulatory system does not appear to be altered by changes in plasma volume or plasma renin as pregnancy progresses.
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Sodium and water retention are normal accompaniments of pregnancy achieved by many significant and complex interrelated alterations in homeostatic forces. Furthermore, potentially harmful derangements in sodium and volume control are found in women with pregnancy-associated hypertension (P-AH, preeclampsia). None of these alterations is completely understood, and many of them appear paradoxical. Recent reviews examined some of the more closely investigated facets of sodium and volume control in normal and hypertensive pregnancy. This relatively brief discussion aims to summarize the known information, update it with more recent work, and speculate on the potential significance of abnormalities in sodium homeostasis in hypertensive pregnancy.
In this chapter are outlined the many factors involved in the regulation of sodium and volume homeostasis in normal human pregnancy and their interrelationships. New developments concerning the role of sodium/potassium ATPase, atrial natriuretic peptide, arginine vasopressin and angiotensin II as regulatory forces are outlined, together with a review of earlier work. Abnormalities found in women with, or destined for, PAH are described and their significance is discussed.
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