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 transient nephrotic syndrome was observed in 24 pregnancies in 23 patients, over a five-year period, in a base hospital obstetric unit. The clinical and biochemical features of this syndrome were similar to the nephrotic syndrome observed in non-pregnant patients. In only half the episodes was the patient a primigravida. In three multigravida patients, previous pregnancies were normal. In 10 of the 24 pregnancies, a perinatal death occurred. A bad fetal prognosis was associated with an early onset of the nephrotic syndrome. Of 11 pregnancies in nine patients occurring after the pregnancy complicated by the transient nephrotic syndrome, seven were normal. One pregnancy was complicated by heavy proteinuria, one by hypertension and intra-uterine death, one by an hydatidiform mole, and one was terminated.
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PMID:The transient nephrotic syndrome of pregnancy. 105 92

The characteristics and treatment of preeclampsia and eclampsia are reviewed. Risk factors for preeclampsia include (1) nulliparity, (2) a mother or sister(s) with a history of the disorder, (3) essential hypertension or renal disease, or (4) a twin or molar pregnancy. Preeclampsia is diagnosed when the systolic blood pressure (BP) increases by 30 mm Hg or the diastolic BP increases by 15 mm Hg after the 20th week of gestation and the BP rise is accompanied by edema, proteinuria, or both. Severe preeclampsia is diagnosed when the BP reaches or exceeds 160 mm Hg systolic or 110 mm Hg diastolic after bed rest. Eclampsia is the occurrence of seizures (in the preeclamptic patient) that cannot be attributed to other causes; it occurs in about 0.2% of preeclamptic patients. Magnesium sulfate (in the injectable, hydrated form) is the agent used most often for seizure prophylaxis in the preeclamptic patient in the United States. It is also used widely to control seizures once they develop. In the United States, diazepam is used to supplement magnesium sulfate if necessary to control seizures, but its use is not routine. Among antihypertensive agents, i.v. hydralazine is preferred in this country to control blood pressure in the severely preeclamptic or eclamptic patient. Several studies provide promising evidence that low-dose aspirin (60-150 mg daily beginning at 28-30 weeks of gestation) prevents preeclampsia in women who are at risk for its development. Until additional comparative studies are completed, magnesium sulfate and hydralazine will remain the standard of care for the treatment of preeclampsia in the United States.
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PMID:Treatment of preeclampsia and eclampsia. 161 13

A toxemia-like syndrome was induced in pregnant beagles by intraperitoneal inoculation of concentrates prepared from placentas of patients with preeclampsia-eclampsia and hydatidiform mole, which contained an agent, Hydatoxi lualba, that stained in a unique fashion with toluidine blue-O-. The pregnant dogs inoculated with either of these concentrates progressively developed hypertension, eyeground changes consistent with hypertensive retinopathy, proteinuria, disseminated intravascular coagulation, and hepatic dysfunction in addition to intrauterine growth retardation and intrauterine fetal death. Hepatic periportal hemorrhage and glomeruloendotheliosis, lesions usually seen in preeclampsia-eclampsia, were also noted to occur in pregnant beagles inoculated with these concentrates. A significant increased sensitivity to angiotensin II infusion was also noted. The toxemia-like syndrome did not develop in pregnant beagles when inoculated in a similar fashion with concentrates prepared from placentas from normal term pregnancies which were free of Hydatoxi lualba or in nonpregnant beagles inoculated with concentrates containing Hydatoxi lualba. Although the agent was not injected in pure form, the inoculation of concentrates containing Hydatoxi lualba appears to be required for the manifestation of the toxemia-like syndrome.
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PMID:Experimental induction of a toxemia-like syndrome in the pregnant beagle. 684 42

Coexistent hydatidiform mole (46, XX) and live fetus (46, XY) in the second trimester is a rare phenomenon. In this case, the clinical manifestations presented as pregnancy-induced hypertension, including hypertension, proteinuria and oliguria. Ultrasonic examination found an enlarged placenta with a typical honeycomb picture, placenta previa and a normal developing fetus. The patient underwent an emergency cesarean section at 23 weeks' gestation on a preliminary diagnosis of acute chorioamnionitis. A 700 g immature male baby was delivered with Apgar scores of 3 at one minute, and 7 at five minutes. The placenta was composed of two parts: one was a molar pregnancy and the other was a normal placenta, both were separated by the membrane. The membrane consisted of one chorion and two amnions. Postmolar persistence of human chorionic gonadotropin was found one month after termination of this pregnancy. Chemotherapy with a single agent (methotrexate) was given. The patient is doing well and has no evidence of recurrence after one year of follow-up.
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PMID:Twin pregnancy with hydatidiform mole (46, XX) and a coexistent fetus (46, XY): report of a case. 791 78

Preeclampsia is a pregnancy-specific condition of increased blood pressure accompanied by proteinuria, edema, or both. The incidence of preeclampsia has been reported as ranging from 2.5% to 7%. Risk factors for the development of preeclampsia include young maternal age, previous preeclampsia, twin pregnancy, chronic hypertension, diabetes mellitus, and hydatidiform mole. Vasospasm is considered central to the pathologic changes of preeclampsia, and the data suggest that this process is triggered by an imbalance between prostacyclin (prostaglandin I2) and thromboxane Ax, biologically active metabolites of arachidonic acid. Preeclampsia has a wide clinical spectrum ranging from mild to severe forms and, potentially, eclampsia with symptoms occurring primarily with severe disease. Preventive strategies under investigation include calcium supplementation and low-dose aspirin supplementation. Prenatal screening, monitoring, and management of preeclampsia are presented.
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PMID:Preeclampsia. 837 57

We treated a 54-year-old woman who was suffering from membranoproliferative glomerulonephritis associated with a complete type of hydatidiform mole. The renal manifestations were proteinuria and hematuria. A renal biopsy, performed before gynecologic management, disclosed focal and segmental subendothelial deposits with a proliferation of the mesangial cell and showed irregularly thickened capillary loops by light and electronmicroscoy. Genralized edema, proteinuria and hematuria were completely recovered by suction and curettage of the hydatidiform mole with prophylactic chemotherapy. The clinical manifestation of earlier presented 3 cases have been the nephrotic syndrome. The common feature of them was a complete remission of the nephropathy after the removal of the hydatidiform mole. The relationship between the hydatidiform mole and glomerulonephritis remains unresolved at present. But we concluded that the hydatidiform mole might be a cause of glomerulonephritis in this case.
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PMID:A case of membranoproliferative glomerulonephritis associated with a hydatidiform mole. 1095 99

The vascular placental pathology (VPP) is associated with many etiologies. Some are the consequence of a maternal genetic or acquired predisposition. Others are associated with a chronic maternal disease (hypertension, lupus, obesity, diabetes, ...). Finally, some others are associated with placental implantation leading to fetal ischemia (multiple pregnancy, chorioangioma, primiparity, feto-placental hydrops) or to environmental (altitude) or nutritional factors (famine and specific alimentary depressions). We classify these factors into three categories according to the risk level (moderate, significant and elevated). While any of these factors can increase the risk of VPP, no one is sufficiently sensitive or specific in predict inevitable onset of VPP. In most cases VPP results from a combination of two (or more) risk factors. The risk factors of VPP classified as moderate include age (> or = 35 years), increased blood pressure during the second trimester of pregnancy, a new paternity, dietetic factors or environmental factors, smoking and controlled diabetes (class B, C), or inactive systemic diseases. Risk is significantly elevated among obese (BMI > or = 25), primiparous women, women with a past familial history (first degree) of preeclampsia or eclampsia, cocaine use or association of tobacco and caffeine use, increased placental mass (associated with twin pregnancy, fetal hydrops or molar pregnancy), uncontrolled diabetes, lupus, active scleroderma. Risk is considered to be high among patients with chronic hypertension, women with a past history of preeclampsia, diabetes (class D, F, R), patients with active systemic disease or with antiphospholipid antibodies or women with lupus or renal lesions and/or proteinuria as well as chronic kidney disease resulting in proteinuria, hypertension and renal insufficiency. Finally, the risk of VPP is considered to be increased in the presence of acquired thrombophilia. It remains moderate in the presence of isolated genetic thrombophilia, except in forms presenting with multiple genetic mutations or associated with an hyperhomocysteinemia. A "high-risk group" is defined among women with past history of deep venous thromboembolic events outside pregnancy, or with a past history of placental vascular pathology (intra-uterine death, placental abruptio, severe and precocious placental, intra-uterine growth retardation, early and repetitive fetal loss) and who, in addition, present with acquired thrombophilia (antiphospholipid antibodies, thrombocytemia), unique homozygous genetic thrombophilia, amultiple genetic thrombophilia or unique heterozygous genetic thrombophilia associated with hyperhomocysteinemia. Prophylactic treatment of acquired thrombophilia and of the multiple genetic forms or associated with hypercysteinemia is a logical rationale, particularly among women with a past history of placental vascular pathology, or with a past history of venous thromboembolic events. On the contrary, prophylaxis using low-molecular-weight heparin in the event of asymptomatic genetic thrombophilic mutations and for women without a past history of deep venous thromboembolism or vascular placental pathology remains controversial.
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PMID:[Vascular placental pathology in high-risk groups: definition and synopsis]. 1502 87

We report the case of 23 years old primingesta patient with a partial molar pregnancy 16 weeks, studying with atypical presentation of preeclampsia (high blood pressure 160/100 mmHg, proteinuria of 3.4 g in 24 hours, headache, photophobia and anasarca), so differential diagnoses ruled out (lupus nephritis, hemolytic uremic syndrome, antiphospholipid antibody syndrome, thrombotic thrombocytopenic purpura, nephrotic syndrome). Disengage vaginally were required by the presence of deterioration of maternal health with systemic repercussions. We observed marked improvement in health status after disengage.
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PMID:[Partial mole and atypical preeclampsia: a case report and review of the literature]. 2340 10

Difficult vaginal deliveries, gynaecological surgery, and, persistent straining during defaecation injure uterine nerves. Cytokines released from injured, uterine nerves cause regeneration of new nerves with altered structures and functions. In structural terms, these new nerves proliferate in chaotic and dysfunctional patterns with abnormal, cross-sectional profiles. In functional terms they are particularly sensitive to "stretch" or mechanosensory transduction. Release of neural cytokines also causes hyperplasia of the walls of adjacent, denervated uterine arterioles that may reduce uteroplacental blood flow during pregnancy. In the "uterine reinnervation" view, "stretch" applied to injured uterine nerves triggers uterorenal nerves to cause vasoconstriction in the renal cortex, hypertension and proteinuria i.e. the key features of preeclampsia. There are two intrauterine mechanisms that stretch injured, uterine nerves (a) in the placental bed, (b) in the extraplacental myometrium, respectively. In "early-onset" preeclampsia (<34weeks), continuing increases in maternal plasma volume, increase blood flow through denervated, and, narrowed uterine arterioles in the placental bed, stretching injured perivascular nerves resulting in preeclampsia with a small-for-gestational-age fetus. In "late-onset" preeclampsia (>34weeks), nulliparity, multiple pregnancy, concealed abruption and polyhydramnios increase myometrial tension and results in preeclampsia with an appropriate-for-gestational-age fetus. Widespread activation of autonomic nerves results in multi-system features of these syndromes. Changes in placental site and circulatory compliance may contribute to different phenotypes of the preeclamptic syndromes in subsequent pregnancies. The "uterine reinnervation" view offers an explanation of the common clinical features of the preeclamptic syndromes through a single pathophysiological mechanism, namely, prepregnancy injury to uterine nerves. Importantly, it offers an explanation for resolution of the symptoms and signs of preeclampsia with delivery of the fetus, the "early" and "late-onset" preeclamptic syndromes, and, the established clinical associations of the condition including nulliparity, hydramnios, multiple pregnancy, molar pregnancy, concealed abruption, etc. Establishing the presence of injured nerves expressing mechanoreceptors in the uterus, and, neural cytokines in thickened, uterine arterioles, will assist in developing this view. However, myometrial hyperplasia during the second half of pregnancy separates injured uterine nerves from injured uterine arterioles ensuring that the key pathoanatomical relationship in preeclampsia will be difficult to demonstrate.
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PMID:Pre-eclampsia - The "uterine reinnervation" view. 2521 51

We would like to know the cause of pre-eclampsia. We would also like to be able to diagnose and treat it quickly and effectively, to be able to predict it accurately with one simple test and prevent it with safe and simple medication. But we cannot, nor on present evidence, will we ever be able to do so. Why is this? There are several reasons, which I will attempt to summarise: the heart of the problem is the complexity and variability of the disorder, which is so daunting that every specific statement about preeclampsia seems to have exceptions - it is truly a disease of exceptions. The cause of pre-eclampsia appears to be the placenta - in that the disorder can occur without a fetus as in hydatidiform mole, without a uterus as in abdominal pregnancy and is resolved by delivery (of the placenta). On the other hand some of the worst presentations are of women who are normal until delivery and then get a major crisis, eclampsia or the HELLP syndrome, immediately afterwards, when the placenta has gone. The placental problem is poor uteroplacental circulation secondary to inadequate remodelling of the spiral arteries that occurs between weeks 8 and week 18 (poor placentation). The maternal symptoms and signs arise from maternal endothelial dysfunction and an associated vascular inflammation. But the placental pathology can occur without features of pre-eclampsia and endothelial dysfunction can arise in mothers without placental disease (maternal pre-eclampsia). This apparent confusion can be resolved in part by recognising that pre-eclampsia is not a disease but a syndrome - encompassed by its defining features of new hypertension and proteinuria that remit after delivery. A syndrome is simply an empirical definition of a clinical presentation that demands action. It tells you nothing about pathogenesis. One syndrome usually encompasses several conditions and this is likely to be true of pre-eclampsia. The key here is to acknowledge that there are many routes to pre-eclampsia; that the final disorder arises from different mixes of environmental and genetic factors, with different contributions from the mother and the placenta. In terms of disease, the unique feature of the latter is that two individuals are involved, mother and baby, each with their different genetic make-ups. This can explain the heterogeneity of pre-eclampsia: for example the difference between early-onset disease with its high preponderance of fetuses that are growth restricted and prominent placental pathology in contrast to the late onset disease, which may be associated with large for gestational age fetuses and routinely reveals little placental pathology. Finally, many very mild features of pre-eclampsia arise towards term in normal healthy women. It is possible that all women are destined to get the disorder. Timing is the key feature, such that late gestation is a race against time: will spontaneous delivery occur before pre-eclampsia or vice versa?
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PMID:Pre-eclampsia: A complex and variable disease. 2610 38


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