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)

A disease characterized by edema, proteinuria, hypoproteinemia and hypertension was seen in late gestation in patas monkeys. The initial sign was edema of the perineum, ankles and lower trunk. The onset was abrupt, occurring 7 days or less prepartum. The affected animals were not depressed, and convulsions were not seen. In 6 of the 98 pregnancies during a 1-year period, symptoms of the disease were present. The highest incidence was manifested by primiparous animals with 3 of 36 pregnancies affected. Two of 38 second pregnancies and 1 of 24 third pregnancies were also affected. Five of the animals recovered spontaneously and were normal 14 days postpartum. Edema persisted for 30 days in one female. This animal continued to be hypertensive and had persistent mild proteinuria and hypoproteinemia. She was killed approximately 1 year postpartum due to severe renal disease. The spontaneous disease seen in patas monkeys resembled toxemia of pregnancy in humans more closely than the experimentally induced disease in other animals.
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PMID:Spontaneous preeclamptic toxemia of pregnancy in the patas monkey (Erythrocebus patas). 10 69

Experimental toxemia of pregnancy was induced in 8 pregnant monkeys (Macacamulatta) by reducing the abdomiinal aorta to one-third of its original diameter during the last month of gestation. It was characterized by hypertension and proteinuria. In the kidney, light and electron microscopy and immunofluorescence revealed findings similar to those in human toxemia. Focal necrosis in the liver and diffuse hemorrhagic infarctions in the placenta were also observed. Plasma renin activity and aldosterone levels, as determined in blood from the uterine vein, were elevated. None of these changes were found in 4 control animals.
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PMID:Experimental toxemia of pregnancy in the monkey, with a preliminary report on renin and aldosterone. 40 16

In order to develop a model for the study of eclamptogenic toxemia, a series of experiments were carried out on 31 female baboons. In Group 1, consisting of 10 animals, metal clips were placed around the uterine arteries in order to partially occlude them, and the ovarian vessels were transected. The animals were subsequently mated. Nine developed hypertension and proteinuria, and one aborted. The renal lesions in these animals were indistinguishable from those described in human toxemia. Group 2 consisted of three of the 10 baboons from Group 1, which became pregnant a second time. They again developed hypertension and proteinuria. In Group 3, three baboons at 100 days of gestation were treated as in Group 1 with similar results. Groups 4 and 5 served as pregnant (3) and nonpregnant (15) controls. It is concluded that a toxemia model has been developed in a subhuman primate. This model will prove useful in the further study of eclamptogenic toxemia.
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PMID:Experimental toxemia in the pregnant primate. 40 66

Toxemia in pregnancy (preeclampsia)is characteristerized by a combination of at least two of the following clinical symptoms: hypertension, edema, and proteinuria. In three successive trials over three consecutive years, the dietary intake of a selected number of young pregnant women attending a Maternal and Infant Care Program at Tuskegee Institute were evaluated for total lipids, individual fatty acids, and cholesterol. Women with toxemia or with any of the individual symptoms were identified and women without toxemia or these symptoms served as controls. Results were variable from repetition to repetition in all but the toxemia group and the edema group. The consumption of total lipids and cholesterol was significantly greater in all three trials by both the toxemia and edema groups. Also, total saturated, monounsaturated, and polyunsaturated fatty acids were eaten in greater amounts. The greatest differences were in palmitic acid, stearic acid, oleic acid, and linoleic acid. The proportion of unsaturated fatty acids consumed in all groups was very low. All differences could be attributed primarily to breakfast and dinner meals and were found in the milk, meat, and egg food groups. Although satistical correlations were found between lipid intake and toxemia of pregnancy any specific relationship between the two is still unclear.
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PMID:Diet-related toxemia in pregnancy. I. Fat, fatty acids, and cholesterol. 47 82

Exacerbation of focal sclerosing glomerulopathy (FSGN) during pregnancy was noted in the three patients. All had antecedent asymptomatic proteinuria. Toxemia developed in two of the women during pregnancy and progressed rapidly to renal failure. Severe nephrotic syndrome developed in one patient with pregnancy and remitted after delivery. These cases suggest a deleterious effect of pregnancy on the course of FSGN and indicate the necessity for doing renal biopsy in women of childbearing age with asymptomatic fixed proteinuria or nephrotic syndrome so that those patients with FSGN can be properly counseled about future pregnancies.
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PMID:Focal sclerosing glomerulopathy with adverse effects during pregnancy. 71 21

The renal biopsies from 123 patients who presented with proteinuria during pregnancy have been reviewed. Forty-seven showed glomerulonephritis that could be diagnosed on morphological grounds or on a clear-cut history of urine abnormalities before pregnancy. Fifty of the remaining 76 had been followed after pregnancy. In these 50 patients, a retrospective diagnosis of glomerulonephritis or preeclamptic toxemia was based on the persistence or disappearance of proteinuria and/or hematuria three or more months after pregnancy. Among 22 in whom a biopsy diagnosis of "pure" preeclamptic toxemia had been made, 19 showed disappearance of urine abnormalities after pregnancy, thus confirming the biopsy diagnosis. A retrospective analysis showed focal and segmental glomeris group but none in the preeclamptic toxemia group. Other differences could not be defined without quantitative evaluation; however, the glomeruli appeared to be more cellular in the glomerulonephritis group. The presence of IgA, IgG, IgM, Complement, and fibrin was not of value in distinguishing glomerulonephritis from preeclamptic toxemia.
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PMID:The differential diagnosis between preeclamptic toxemia and glomerulonephritis in patients with proteinuria during pregnancy. 100 33

Experimental toxemia of pregnancy was induced in 51 of 122 rabbits by constriction of the aorta below the renal arteries. The approach was extraperitoneal and dependent on the accuracy in calibrating this stricture between 0.6 and 1.0 mm. Experimental toxemia in the rabbit was characterized by hypertension, proteinuria, weight gain, and reduced weight of the fetus. Blood pressure and blood flow studies distal to the aortic constriction demonstrated a marked diminution of blood supply below the constriction. The light microscopic changes in the kidneys and in the liver were similar to those of human toxemia. The electron microscopic changes consisted of endothelial swelling and subendothelial deposits. In a separate experiment, 22 pregnant rabbits near term had an aortic constriction varying between 0.6 and 1.0 mm. This constriction lasted 4 to 12 days. Glomerular deposits of fibrinogen were demonstrated by immunofluorescence in 20 of 22 animals. The intensity of the immunofluorescence was related to the severity and duration of the aortic stricture.
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PMID:Production of experimental toxemia in the pregnant rabbit. 125 1

A better understanding of the hemodynamic abnormalities in gestational hypertension together with the use of effective antihypertensive agents have resulted in more rational therapeutic approaches and a substantial improvement in maternal and fetal welfare. In normal pregnancy, there is reduced vascular reactivity with peripheral pooling and decreased circulatory responses to pressor agents. These are prostacyclin-dependent processes. In gestational hypertension, the normal increase in plasma volume and cardiac output with pregnancy is attenuated and prostacyclin-dependent processes are impaired, resulting in persistent vasoconstriction, enhanced responses to pressor agonists, and failure to develop adequate uteroplacental interchange. Among the modern antihypertensive agents, alpha- and beta-adrenergic antagonists and calcium ion entry blockers have permitted safe and effective long-term blood pressure control with sustained fetal growth. The development of proteinuria that can occur in chronic hypertension or in previously normotensive women (toxemia of pregnancy) can be prevented by the use of beta-adrenergic blocking agents and possibly by low-dose aspirin (75 mg/day). Maternal prostacyclin-thromboxane imbalance, important in the pathogenesis of gestational hypertension, is corrected by low-dose aspirin treatment. With the prevention of pre-eclampsia, the adverse maternal and fetal prognosis in gestational hypertension has been improved.
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PMID:Treatment of hypertension in pregnancy. 170 7

Architectural changes in placental villi in clinical types of toxemia of pregnancy which were divided into four groups according to the main maternal symptoms (hypertension: H type, proteinuria: P type, PH type and IUFD) were studied by scanning electron microscopy and computerized image analysis of serial paraffin step sections. Furthermore plastic casts of villous capillaries were compared and changes in endothelial cells of villous capillaries were observed by transmission electron microscopy. 1) Scanning electron microscopy showed characteristic differences between P type cases and H type cases. Terminal villi were markedly reduced in number and showed few branches especially in P type cases, whereas in H type cases slender terminal villi were observed. The surface structure showed rough degenerative microvilli in H type cases and slender long microvilli in P type cases. 2) Average diameters of terminal branches estimated by image analysis were as follows: Normal cases: 24.8 mu, P type: 23.1 mu, H type: 17.9 mu, PH type: 17.7 mu, IUFD: 13.8 mu. The reduction in the number of intermediate villi in cases of toxemia of pregnancy was about 58% of that of normal cases. 3) Plastic casts of villous capillaries emphasized these changes in each type. 4) Swelling of the endothelial cell into the capillary lumen was observed and an increase in the number of filamentous structures in the cytoplasm of endothelial cells was detected by transmission electron microscopy.
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PMID:[Study on the stereo-architectural changes in human placental villi of toxemia of pregnancy]. 199 20

Genetical differences in changes in blood pressure (BP) were chronologically investigated during pregnancy in stroke-prone spontaneously hypertensive rats (SHRSP), Wistar-Kyoto rats (WKY) and Sprague-Dawley (SD) rats. Especially, the early stages were carefully studied. Maternal conditions in SHRSP were modified by the treatments with NaCl and taurine, respectively. BP in SHRSP and WKY rose significantly at the early stage of pregnancy compared to prepregnancy levels (SHRSP; 208 +/- 2 mmHg vs 197 +/- 5 mmHg, WKY; 133 +/- 2 mmHg vs 126 +/- 1 mmHg) (p less than 0.05). In contrast, no such changes were observed in SD rats. Differences in 24-hour urinary epinephrine excretion before and during pregnancy ran parallel with such BP changes among these strains. NaCl-loaded SHRSP died during pregnancy with severe pathohistological changes in their kidneys and severe proteinuria. Taurine treatment had a marked prophylactic effect on these maternal pathological changes during pregnancy, resulting in better growth in offsprings. These results suggest that SHRSP could be one of the suitable animal models for the studies on toxemia of pregnancy and also suggest an important role of hypertensive genetical disposition in the development of toxemia of pregnancy.
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PMID:Stroke-prone spontaneously hypertensive rats as a model for toxemia of pregnancy and aggravating and preventive effects of maternal modifications during pregnancy on offspring's growth. 223 19


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