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Insulin resistance and hyperinsulinemia are associated with essential hypertension. There is also evidence of hyperinsulinemia in women who developed hypertension in pregnancy (P). The present study examines whether chronic hyperinsulinemia in pregnant rats plays a role in the development of hypertension in pregnancy. A sustained-release insulin pellet was implanted subcutaneously in 15 Wistar rats (P-INS) 1 wk before and on day 7 of pregnancy; 14 control rats were sham-implanted (P-SHAM). Tail-cuff systolic BP (SBP), serum triglycerides, glucose, insulin, renal function, and urinary excretion of Na+ and of metabolites of nitric oxide were determined throughout pregnancy. Data were analyzed by ANOVA with basal body weight as covariate analysis of covariance. Results are expressed as the mean +/- SD. Body weight; water and food intake; urine volume; creatinine clearance; and level of proteinuria at the end of pregnancy were similar in both groups. The number of fetuses was 9 +/- 2.3 in P-INS versus 11 +/- 2.4 in pregnant control rats (P < 0.05). Before mating, SBP was similar, but at the end of pregnancy SBP was 110 +/- 18 mmHg in P-INS versus 85 +/- 12 mmHg in pregnant rats (P < 0.05). Serum triglycerides and Na+ were also higher in P-INS rats. The fractional excretion of Na+ was 3.1 +/- 1.0 versus 4.4 +/- 1.5, respectively (P < 0.01). The percent increase in nitric oxide metabolite excretion was 233 +/- 14 versus 370 +/- 17%, respectively (P < 0.01). Chronic hyperinsulinemia, without sugar supplementation, and hypertriglyceridemia may cause a decrease in the synthesis of nitric oxide in P-INS rats. The development of hypertension in these rats may be associated with an impaired vasodilatation, together with an increased renal sodium reabsorption.
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PMID:Chronic exogenous hyperinsulinemia in pregnancy: a rat model of pregnancy-induced hypertension. 944 81

Beta2-Microglobulin (beta2-m) is a polypeptide that is freely filtered and then mostly reabsorbed and degraded in the proximal renal tubule. Beta2-m is a marker of glomerular filtration (GFR) in renal failure, whereas urinary beta2-m is a marker of proximal renal tubular dysfunction. Preeclampsia (PE) (ie, de novo hypertension in pregnancy with accompanying renal, cerebral, or liver disease or thrombocytopenia) often has renal involvement characterized by proteinuria, decreasing glomerular filtration, or renal tubular dysfunction. The aim of this study was to determine whether serum beta2-m concentration or urinary beta2-m excretion were greater in women with PE than in women with gestational hypertension (GH) (ie, isolated de novo hypertension in the second half of pregnancy) and normal pregnant women. Seventy-five pregnant women (35 with PE, 22 with GH, and 18 normotensives) were studied prospectively. Serum creatinine and beta2-m concentrations, 24-hour proteinuria, and fractional excretion (FE) of beta2-m were measured. Preeclamptics had similar serum creatinine but higher serum beta2-m (3.26+/-0.99 mg/L) than gestational hypertensives (2.44+/-0.77 mg/L; P = 0.016), and both groups had higher serum beta2-m than controls (1.62+/-0.54 mg/L; P = 0.001). FE of beta2-m was similar amongst groups (PE: 0.27%; interquartile range [IQR]: 0.20-0.86; GH: 0.21%; IQR: 0.11-0.40; controls: 0.26%, IQR: 0.12-0.69). PE is characterized by higher serum beta2-m but similar serum creatinine to GH. Because FE beta2-m is similar in these groups, this implies reduced filtering of beta2-m in PE rather than altered tubular handling of beta2-m. Further studies are now necessary to assess whether measurement of serum beta2-m is helpful in the clinical management of the hypertensive disorders of pregnancy.
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PMID:Beta2-microglobulin in hypertensive pregnancies. 946 2

Hypertension in pregnancy is defined by a systolic blood pressure > or = 140 mm Hg and a diastolic blood pressure of > or = 90 mm Hg or by a rise in blood pressure of systolic > or = 30 mm Hg and diastolic > or = 15 mm Hg. High blood pressures are found in 5-10% of all pregnancies. The outcome of pregnancy is influenced by the fact whether there occurs a proteinuria in addition to hypertension. While the prognosis of an isolated hypotension is good, the combination of hypertension and proteinuria leading to preeclampsia is the primary cause of maternal death in many countries and is responsible for 20-25% of perinatal mortality. A simple classification divides between chronic hypertension, preeclampsia, preeclampsia superimposed on chronic hypertension and transient hypertension. With chronic hypertension pregnancy outcome is determined by a preexisting nephropathy and the occurrence of a superimposed preeclampsia. Preeclampsia and superimposed preeclampsia are pregnancy induced multiorganic diseases, endangering both the mother and the fetus. Transient hypertension is a benign pathology, which occurs toward the end of pregnancy usually on the basis of a latent essential hypertension, which is laid open through pregnancy. While a severe chronic hypertension in pregnancy must be treated to prevent a hypertensive maternal encephalopathy, a less severe chronic hypertension should not be treated as the risk of a superimposed preeclampsia and the maternal and fetal outcome cannot be influenced by antihypertensive therapy. The incidence of preeclampsia is 3-5% in nulliparae and 0.5% in multiparae. Preeclampsia is a severe and dangerous pathology with an unknown etiology. Pregnancy termination is the only causal therapy. At present it is still recommended to terminate a severe preeclampsia after stabilizing the mother, irrespective of gestational age. In less severe preeclampsia occurring before 32 weeks of gestation, termination of pregnancy can be postponed under intensive monitoring and a prophylaxis with magnesium sulfate in order to accelerate the fetal lung maturation with glucocorticoids. A conservative management in the case of a HELLP-syndrome (Haemolyis, Elevated Liver enzymes, Low Platelets), which is a very severe form of preeclampsia, is not recommended because it hasn't been validated in prospective controlled studies. The most dangerous complication of preeclampsia is eclampsia, which is defined by general tonic-clonic convulsions before or after birth. The most effective prophylaxis of eclamptic attacks is the intravenous therapy with magnesium sulfate. A primary prohylaxis for preeclampsia doesn't exist. Treatment with low-dose aspirin in high-risk patients, i.e. after a severe preeclampsia, in cases of chronic hypertension, in cases of nephropathy and in cases with antiphospholipid-syndrome++ can be recommended. The prophylactic use of low-dose heparin, which has lead to a significant decreased incidence of preeclampsia in retrospective analysis, is now the object of a randomized, controlled trial in our hospital. All women who suffered from a preeclampsia should have a check-up after 3-6 months. Preexisting pathologies are found in up to 40% of patients, mostly in multiparae, i.e. chronic hypertension, nephropathy, endocrine pathologies, anomalies of blood coagulation and antiphospolipid-syndrome.
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PMID:[Hypertensive disorders in pregnancy]. 1054 28

In many ways there should be no need to classify hypertensive disorders in clinical practice. The very presence of rising blood pressure should alert the clinician to seek evidence for the development of pre-eclampsia and whether there are any emerging abnormalities of fetal growth and/or maternal renal, cerebral, hepatic or coagulation functions which may necessitate specific treatment, including delivery. While such a view may be appropriate for experienced clinicians with an understanding of the pathophysiology of the hypertensive disorders of pregnancy, it is of little help to junior or less experienced medical staff. Moreover, without an agreed international classification system it is impossible to compare truly clinical outcome, intervention or basic research studies from different units as entry criteria to these studies may differ considerably across individual units and certainly across countries. In this chapter we highlight the limitations of the existing classification systems and propose a system that is based on our present understanding of the pathophysiology of pre-eclampsia. The proposed system is not a radical departure from previous classifications, with grouping of hypertensive subjects into gestational hypertension, pre-eclampsia and chronic (usually essential) hypertension. Proteinuria, while remaining a hallmark of pre-eclampsia, is no longer considered a 'sine qua non' for this disorder to be diagnosed, reflecting our greater understanding of the maternal and fetal abnormalities in pre-eclampsia since previous classification systems were developed. This classification system has been compared with the traditional system of diagnosing proteinuric pre-eclampsia in a study of 1183 women with hypertension in pregnancy: diagnosing pre-eclampsia in this new manner still stratifies a high-risk group of pregnant women and the proposed diagnosis of gestational hypertension in this system stratifies a group of women at low maternal and fetal risk, provided that continual maternal and fetal monitoring is employed. We hope that this system of classification can be adopted uniformly, permitting appropriate triage of pregnant women into higher and lower clinical risk groups while allowing us to compare 'apples with apples' in future research studies.
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PMID:Classification of hypertension in pregnancy. 1074 91

Hypertension is found among 1 to 6% of young women. Treatment aims to decrease cardiovascular risk, the magnitude of which is less dependent on the absolute level of blood pressure (BP) than on associated cardiovascular risk factors, hypertension-related target organ damage and/or concomitant disease. Lifestyle modifications are recommended for all hypertensive individuals. The threshold of BP at which antihypertensive therapy should be initiated is based on absolute cardiovascular risk. Most young women are at low risk and not in need of antihypertensive therapy. All antihypertensive agents appear to be equally efficacious; choice depends on personal preference, social circumstances and an agent's effect on cardiovascular risk factors, target organ damage and/or concomitant disease. Although most agents are appropriate for, and tolerated well by, young women, another consideration remains that of pregnancy, 50% of which are unplanned. A clinician must be aware of a woman's method of contraception and the potential of an antihypertensive agent to cause birth defects following inadvertent exposure in early pregnancy. Conversely, if an oral contraceptive is effective and well tolerated, but the woman's BP becomes mildly elevated, continuing the contraceptive and initiating antihypertensive treatment may not be contraindicated, especially if the ability to plan pregnancy is important (e.g. in type 1 diabetes mellitus). No commonly used antihypertensive is known to be teratogenic, although ACE inhibitors and angiotensin receptor antagonists should be discontinued, and any antihypertensive drugs should be continued in pregnancy only if anticipated benefits outweigh potential reproductive risk(s). The hypertensive disorders of pregnancy complicate 5 to 10% of pregnancies and are a leading cause of maternal and perinatal mortality and morbidity. Treatment aims to improve pregnancy outcome. There is consensus that severe maternal hypertension (systolic BP > or = 170mm Hg and/or diastolic BP > or = 110mm Hg) should be treated immediately to avoid maternal stroke, death and, possibly, eclampsia. Parenteral hydralazine may be associated with a higher risk of maternal hypotension, and intravenous labetalol with neonatal bradycardia. There is no consensus as to whether mild-to-moderate hypertension in pregnancy should be treated: the risks of transient severe hypertension, antenatal hospitalisation, proteinuria at delivery and neonatal respiratory distress syndrome may be decreased by therapy, but intrauterine fetal growth may also be impaired, particularly by atenolol. Methyldopa and other beta-blockers have been used most extensively. Reporting bias and the uncertainty of outcomes as defined warrant cautious interpretation of these findings and preclude treatment recommendations.
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PMID:Treating hypertension in women of child-bearing age and during pregnancy. 1136 52

Fifty per cent of pregnancies are unplanned, and 1-6% of young women have pre-existing hypertension. However, no commonly used antihypertensive agent is known to be teratogenic. ACE inhibitors (and angiotensin-receptor antagonists) should be discontinued due to fetotoxicity. Five to 10% of pregnant women have hypertension, of which pre-existing hypertension is but one type. There is consensus that severe maternal hypertension (blood pressure >or=170/110 mmHg) should be treated to minimize the risk of acute cerebrovascular complications. Parenteral hydralazine may be associated with a higher risk of maternal hypotension, and intravenous labetalol with neonatal bradycardia. There is no consensus that mild-to-moderate hypertension in pregnancy should be treated. Clinical trials indicate that transient severe hypertension, antenatal hospitalization, proteinuria at delivery and neonatal respiratory distress syndrome may be decreased by normalizing blood pressure, but intrauterine fetal growth restriction may be increased. Methodological problems with published trials warrant cautious interpretation of these findings. Methyldopa and beta-blockers have been used most extensively, although atenolol may impair fetal growth in particular and should be avoided.
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PMID:Drugs in pregnancy. Antihypertensives. 1180 May 27

With the objective to assess the prognostic value of office values as compared with ambulatory monitoring in pregnancy, we analyzed 2430 blood pressure series systematically sampled from 403 untreated pregnant women for 48 consecutive hours every 4 weeks from the first visit to the hospital until delivery. Women were divided into 5 groups: "detected" gestational hypertension, women with office blood pressures >140/90 mm Hg after 20 weeks of gestation and hyperbaric index (area of blood pressure excess above the upper limit of a time-specified tolerance interval) consistently above the threshold for diagnosing hypertension in pregnancy; "undetected" gestational hypertension, office values <140/90 mm Hg but hyperbaric index above the threshold for diagnosis; normotension, both office values and hyperbaric index below the thresholds for diagnosis; white coat hypertension, women with recorded diagnosis of gestational hypertension but hyperbaric index consistently below the threshold for diagnosis; and preeclampsia, defined as gestational hypertension and proteinuria. Results indicate small and nonsignificant differences in 24-hour mean of ambulatory pressures between "detected" and "undetected" gestational hypertension at all stages of pregnancy, in contrast with highly significant differences between these two groups and normotensive pregnancies. Average office blood pressure values were similar for preeclampsia, "detected," and "undetected" gestational hypertension. The hyperbaric index was, however, significantly higher for women with preeclampsia after 20 weeks of gestation as compared with all other groups and higher for women with either "detected" or "undetected" gestational hypertension as compared with normotensive pregnant women. The incidence of preterm delivery and intrauterine growth retardation were similar for "detected" and "undetected" gestational hypertension but significantly lower for normotensive women. In pregnancy, the hyperbaric index derived from ambulatory monitoring is markedly superior to office measurements for diagnosis of what should be truly considered gestational hypertension, as well as for prediction of the outcome of pregnancy.
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PMID:Prognostic value of office and ambulatory blood pressure measurements in pregnancy. 1221 70

This study evaluated the prognostic value of absolute versus relative rise in blood pressure during pregnancy at the Department of Obstetrics and Gynaecology, University of Nigeria Teaching Hospital, Enugu, Nigeria from 17th December 1997 to 31st March 1999. The study sample consisted of 515 consecutive healthy antenatal subjects of the hospital who satisfied the inclusion criteria. The study involved a longitudinal measurement of variables such as blood pressure and anthropometric data of the subjects as well as the maternal mortality rate, caesarean section rate, incidence of eclampsia and proteinuria, perinatal mortality rate, incidence of severe asphyxia and low birth weight, mean birth weight, birth length, ponderal index and gestational age at delivery. Differences in these indices between different groups of the subjects were compared using the chi-square test for categorical variables and one way ANOVA for continuous variables. Grouping was based on the absolute systolic/diastolic blood pressure (SBP/DBP) and relative rise in SBP/DBP from mind-pregnancy until delivery at term. The absolute blood pressure of 140/90 mmHg was a better predictor of feto-maternal outcome than a relative rise in the systolic/diastolic blood pressure from mid pregnancy, which did not reach this absolute level. We conclude that in the Nigerian obstetric population, the practice of diagnosing pregnancy hypertension on the basis of a relative blood pressure rise of 30/15 mmHg alone without reference to the absolute blood pressure level needs to be reviewed.
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PMID:Prognostic value of absolute versus relative rise of blood pressure in pregnancy. 1247 27

BACKGROUND: Hypertensive disorders in pregnancy are leading causes of maternal, fetal and neonatal morbidity and mortality worldwide. However, studies attempting to quantify the effect of hypertension on adverse perinatal outcomes have been mostly conducted in tertiary centres. This population-based study explored the frequency of hypertensive disorders in pregnancy and the associated increase in small for gestational age (SGA) and stillbirth. METHODS: We used information on all pregnant women and births, in the Canadian province of Nova Scotia, between 1988 and 2000. Pregnancies were excluded if delivery occurred < 20 weeks, if birthweight was < 500 grams, if there was a high-order multiple pregnancy (greater than twin gestation), or a major fetal anomaly. RESULTS: The study population included 135,466 pregnancies. Of these, 7.7% had mild pregnancy-induced hypertension (PIH), 1.3% had severe PIH, 0.2% had HELLP (hemolysis, elevated liver enzymes, low platelets), 0.02% had eclampsia, 0.6% had chronic hypertension, and 0.4% had chronic hypertension with superimposed PIH. Women with any hypertension in pregnancy were 1.6 (95% CI 1.5-1.6) times more likely to have a live birth with SGA and 1.4 (95% CI 1.1-1.8) times more likely to have a stillbirth as compared with normotensive women. Adjusted analyses showed that women with gestational hypertension without proteinuria (mild PIH) and with proteinuria (severe PIH, HELLP, or eclampsia) were more likely to have infants with SGA (RR 1.5, 95% CI 1.4-1.6 and RR 3.2, 95% CI 2.8-3.6, respectively). Women with pre-existing hypertension were also more likely to give birth to an infant with SGA (RR 2.5, 95% CI 2.2-3.0) or to have a stillbirth (RR 3.2, 95% CI 1.9-5.4). CONCLUSIONS: This large, population-based study confirms and quantifies the magnitude of the excess risk of small for gestational age and stillbirth among births to women with hypertensive disease in pregnancy.
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PMID:The effect of hypertensive disorders in pregnancy on small for gestational age and stillbirth: a population based study. 1529 17

Maternal hypertension and proteinuria after 20 weeks gestation defines preeclampsia. Severe preeclampsia is defined by severe hypertension or massive proteinuria, with or without symptoms or altered laboratory tests. With an incidence of 4-7%, preeclampsia remains a major cause of maternal and neonatal morbidity and mortality. Admission into a hospital is crucial to monitor both mother and fetus. The only treatment is delivery. Management of blood pressure and prevention of eclampsia with magnesium sulfate is indicated in severe preeclampsia. Despite numerous studies attempting to elucidate the exact etiopathogenesis of this complex multifactorial disease, prediction or prevention of preeclampsia is not available. Preeclampsia has been named the "disease of theories" and remains to date a challenging enigma for the scientific community.
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PMID:[Recent data on the physiopathology of preeclampsia and recommendations for treatment]. 1577 58

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