Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cholesterol:phospholipid ratio (C/PL) was measured in platelet plasma membrane in patients with pregnancy-induced hypertension [with proteinuria (PE), and without proteinuria (PIH)] and in matched normotensive gestational controls (NT). The C/PL was raised in the platelet membrane from PE (1.52 +/- 0.50, 95% CI 1.13 to 1.90) and PIH (1.38 +/- 0.34, 95% CI 1.08 to 1.67) compared with that from NT controls (0.88 +/- 0.13, 95% CI 0.80 to 0.95) (p less than 0.01, ANOVA test). No correlation was found when C/PL was regressed against total serum cholesterol levels. The abnormality of lipid composition of the platelet plasma membrane could account for some of the changes in platelet function that have been described in PIH.
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PMID:Abnormal platelet lipid membrane composition in pregnancy induced hypertension. 150 Oct 54

Pregnancy-induced hypertension is a disorder of unknown etiology unique to pregnant women. Classic clinical manifestations include hypertension, proteinuria, and edema. Early recognition and proper management of this disease may serve to avoid serious maternal complications. Ultimate maternal treatment depends on delivery of the fetus and placenta. Advanced stages of this disease result in multi-organ system dysfunction that may be life-threatening to the mother and her fetus. Such maternal complications of PIH include severe hypertension, oliguria or anuria, HELLP syndrome, eclamptic seizures, liver rupture, pulmonary edema, cerebral edema, and abruptio placentae. A multidisciplinary approach of the critical care team often will effect a reduction in maternal morbidity and mortality.
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PMID:Management of severe preeclampsia and eclampsia. 174 3

A retrospective study was made to determine the incidence of pregnancy-induced hypertension (PIH, pre-eclampsia) in Iceland. One-fourth of all births in Iceland in 1985 were selected from the national birth registry files by random number allocation, a total of 904 women. Maternity records were found in 97.9% of the cases. The criteria used to define PIH were met in 17.4% of the women. There were 146 (16.5%) with mild PIH (blood pressure of greater than or equal to 140/90 mmHg with or without proteinuria after the 20th gestational week). Eight (0.9%) had severe PIH (blood pressure of greater than or equal to 160/110 mmHg with or without proteinuria after the 20th gestational week). Primigravid women formed one-third of the group and of these 20.9% had PIH compared with 15.4% of the parous women. The incidence in parous women was higher than usually reported.
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PMID:Incidence and relation to parity of pregnancy-induced hypertension in Iceland. 263 27

Hypertensive diseases represent the most frequent disorders among medical complications of pregnancy. Numerous studies have proven the central role of prostaglandins in these complex diseases. Thus, determination of urinary prostaglandins may lead to a better understanding of the pathomechanismus and may be a basis for therapeutic approaches. Our study included 59 patients with pregnancy-induced hypertension. From these 18 women had a proteinuria > 300 mg/l and were classified as pre-eclamptic. As controls 53 normotensive pregnancies were investigated. Quantification of 6-keto-PGF1 alpha, 2,3-dinor-6-keto-PGF1 alpha, TxB2, 11-Dehydro-TxB2 and PGE2 was performed with radio or enzyme immunoassays after purification with solid phase extraction and partly HPLC. In the third trimester of pregnancy following alterations were found in urine concentrations of prostaglandins in preeclamptic women compared to controls: 6-keto-PGF1 alpha - 54%, 2,3-dinor-6-keto-PGF1 alpha - 29%, PGE beta 2-41%, TxB2-29% and 11-Dehydro-TxB2 + 21%. Thus, our results show a disturbed balance between vasodilatory and vasoconstrictive prostaglandins in PIH patients. This imbalance correlated to the severity of the disease and was more pronounced in preeclamptic patients. The decrease of PGI2- and PGE2-production was more distinct than the increase of thromboxane production. We conclude that the endothelial damage, rather than an overproduction of TxA2 predominantly is responsible for some pathophysiological events in PIH.
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PMID:[Prostaglandins in the urine of hypertensive pregnant patients]. 804 88

This review on hypertension in pregnancy focuses mainly on the pathophysiology and prevention of pregnancy induced hypertension which, when associated with proteinuria, is usually called preeclampsia. Rather than a genuine hypertensive disease, preeclampsia is mainly a systemic endothelial disease causing activation of platelets and diffuse ischemic disorders whose most obvious clinical manifestations involve the kidney (hence the proteinuria, edema and hyperuricemia), the liver (hence the hemolytic elevated liver enzymes and low platelets, or HELLP syndrome), and the brain (hence eclamptic convulsions). Hypertension is explained by increased vascular reactivity rather than by an imbalance between vasoconstrictive and vasodilating circulating hormones. This increased reactivity is due to endothelial dysfunction with imbalance between prostacyclin and thromboxane A2 and possibly dysfunction of NO and endothelin synthesis. The aggressive substances for endothelium are thought to be of placentar origin and the cause of their release is explained by placentar ischemia related to a defect of trophoblastic invasion of the spiral arteries. The etiology of this latter defect is unknown but involves immunologic mechanisms with genetic predisposition. The only effective treatment for PIH is extraction of the baby with the whole placenta. The decision for extraction is often a very delicate obstetric problem. Antihypertensive drugs are mainly indicated in severe hypertension (> 160-100 mm Hg), with the aim of preventing cerebral hemorrhage in the mother, but have not been shown to improve fetal morbidity or mortality. Eclamptic seizures can be prevented and treated more effectively with magnesium sulfate than with diazepam or phenytoin. Prevention of preeclampsia remains the main challenge. Whereas antihypertensive drugs are ineffective, calcium supplementation and low dose aspirin have proven effective but mainly in selected populations with a relatively high incidence of preeclampsia (> 8-10%). In multiparas the selection of such a high risk population is relatively easy when at least 2 (or 1?) previous pregnancies were complicated with early preeclampsia and/or intrauterine growth retardation. In nulliparas the selection of the high-risk population is still a subject of research. The 2 most promising criteria are abnormal Doppler velocimetry of the uterine arteries at around 20 weeks of amenorrhea, and abnormally high plasma levels of beta HCG at 17 weeks of amenorrhea.
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PMID:[Hypertension and pregnancy. Diagnosis, physiopathology and treatment]. 853 76

Serum uric acid estimation was done in forty primigravidae with pregnancy induced hypertension and twenty normotensive primigravida in the third trimester of pregnancy, at delivery and six weeks postpartum. The mean serum uric acid levels in normotensive women in the antenatal period and at delivery were 4.65 +/- 0.33 and 4.88 +/- 0.23 mg% and in mild PIH were 5.42 +/- 0.55, 6.14 +/- 0.76 mg%, respectively. Level of serum uric acid in mild PIH was significantly higher than normotensive women (P). In severe PIH, the mean serum uric acid levels were 6.65 +/- 0.60, 8.24 +/- 1.09 mg% in antepartum and at delivery respectively which was significantly more than control group and mild PIH group women (P). However, no differences was observed, in the serum uric levels between these groups during the postpartum period. Serum uric acid level of 5.5 mg or more was observed to be an indicator of PIH. Levels of serum uric acid did show a high positive correlation with the severity of PIH in relation to hypertension and proteinuria. Hyper uricemia (more than 5.5 mg% is associated with increased perinatal morbidity and mortality.
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PMID:Hyperuricemia and pregnancy induced hypertension--reappraisal. 897 21

Study group consisted of 63 women in the III trimester of pregnancy (gestational age 29-40 weeks). 32 subjects with PIH (investigated group) were compared to control group consisted of 30 healthy patients with uneventful course of gestation. Women with PIH had no proteinuria nor oedema, their mean blood pressure remained at the level of 161 +/- 16.7/98 +/- 12.8 mm Hg. Concentration of calcium, phosphorus and magnesium in serum blood and urine were determined. It was stated that due to renal impairment observed during PIH, calcium urine excretion and calcium concentration in blood serum are decreased while serum inorganic phosphorus levels are increased. No changes in magnesium and ionised calcium homeostasis were seen in the course of PIH.
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PMID:[Homeostasis of calcium-phosphorus-magnesium in women with pregnancy induced hypertension]. 928 28

Among 244 pregnant with diabetes type 1 in 21 (8.61%) cases nephropathy was noticed, which was accompanied by such complications as: retinopathy--85.7%, H.A.--42.9%, PIH--28.6%, anaemia--42.9%. During the course of pregnancy statistically significant increase of biochemical parameters such as: proteinuria, serum urea and creatinine levels was noticed. Preterm delivery represented 66.6% (the average delivery time approximately 33 week of the pregnancy), IUGR appeared in 26.3% of cases, and neonatal mortality was equal 15.9%. The proteinuria amount was negatively correlated with neonatal birth weight similarly as the pregnant serum urea level was negatively correlated with Apgar score.
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PMID:[Pregnancy in women with diabetic nephropathy]. 1108 44