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 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expanded toxemia syndrome or gestosis refers to polysymptomatic diseases that are associated with pregnancy. This report discusses those cases without initial hypertension or proteinuria that were "cured" by delivery and were associated with maternal and fetal morbidity (usually intrauterine growth retardation). A list of suggested tests is presented to document gestosis in pregnant women with medical illnesses. Unlike preeclampsia, gestosis may occur at almost any time in pregnancy.
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PMID:Expanded toxemia syndrome or gestosis. 371 33

Plasma PRL levels were measured in 111 normal pregnant women and in 21 patients with severe toxemia of pregnancy. Twelve of 21 patients with severe toxemia of pregnancy showed high PRL levels in zone A (greater than mean value + 1 S.D. of PRL values in normal pregnancy). These 12 were significantly lower (P less than 0.02) in the Ccre rate, at 70.2 +/- 19.2 ml/min, than 5 toxemia patients (101.4 +/- 26.7 ml/min) in zone B (mean + 1 S.D. approximately mean) and 4 toxemia patients (110.0 +/- 35.3 ml/ml) in zone C (mean approximately mean -1 S.D.). Also, BUN, proteinuria and uric acid levels in zone A patients were higher than in those in zone B and C. However, no correlation was found between PRL levels and mean diastolic and systolic blood pressure. These results suggest that high PRL concentrations in toxemia of pregnancy may be associated with renal dysfunction.
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PMID:Prolactin in severe toxemia of pregnancy. 378 Oct 70

This study reviews liver disease in toxemia of pregnancy based on 102 cases submitted to the Armed Forces Institute of Pathology. The common clinical features were right upper quadrant and epigastric pain, nausea, vomiting, and elevation of the serum transaminases. Jaundice occasionally developed. These occurred in severe preeclampsia or eclampsia and their cause was usually recognized. However, hepatic symptoms and signs did result in inappropriate diagnoses and misdirected therapy. Such confusion occurred when these were the initial problems confronting the clinician in women presenting with advanced toxemia due to poor prenatal care. They were also likely to be misleading when other more classic parameters, such as blood pressure and proteinuria, were only midly abnormal. Central nervous system complications were the common cause of death but liver disease could be partially or wholly responsible. Extensive periportal lesions, hepatic hematomas, spontaneous rupture, and infarction all contributed to hepatic injury and to morbidity. Fibrin deposition, hemorrhage, or both in the periportal areas was characteristic of the histopathology. Scanning electron microscopy validated this spectrum of change. A toxemic vasculopathy related to severe vasospasm in the hepatic arterial circulation may be responsible.
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PMID:Liver disease in toxemia of pregnancy. 378 23

Vesicoureteral reflux (VUR) is mainly a primary phenomenon due to incompetence of the ureterovesical junction, mostly affecting a pediatric population. During micturition cystourethrography (MCU) reflux into the kidney--intrarenal reflux (IRR)--is occasionally seen. In areas with IRR the kidney surface may subsequently be depressed and the papillae retracted (reflux nephropathy (RN]. VUR may lead to hypertension and/or end-stage renal failure. Most commonly, VUR is discovered during evaluation for urinary tract infection, but it may also be present in patients with hypertension, toxemia of pregnancy, chronic renal failure and proteinuria, and it may be found in siblings of patients with VUR. For the time being VUR is demonstrated at radiographic MCU, whereas RN is diagnosed by demonstration of focal scars and of abnormal parenchymal thickness at urography. In children with VUR and no abnormalities of calyces or parenchymal defects standardized measurement of the parenchymal thickness at three sites may identify kidneys which are likely to develop focal scars. Quantitation of focal scarring should be performed in connection with a measure of the overall kidney size. The occurrence of IRR is dependent of the papillary morphology, intrapelvic pressure and urine flow. There may be an important relationship between renal ischemia and IRR in producing a 'vicious circle of deleterious effects' which, combined with parenchymal extravasation, may lead to RN. Treatment of VUR includes medical and surgical management. Since renal scarring may occur in infancy, prevention should focus on infants and young children. Infants and young children with severe VUR may have normal urograms. Therefore a MCU should also be performed, preferably with the recommended standardized technique.
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PMID:Vesicoureteral reflux and reflux nephropathy. 388 98

Toxemia was induced in 13 of 20 pregnant ewes by the stress of a change in environment and food deprivation late in pregnancy. Of the toxemic ewes, eight developed prominent neurological findings with convulsions, motor weakness, and blindness, whereas five ewes developed azotemia without neurological signs. Proteinuria and azotemia occurred in all but one of the toxemic animals. Seven animals did not develop clinical or laboratory evidence of toxemia. Hypertension did not occur with the onset of toxemia but all toxemic animals showed glomerular changes by light and electron microscopy. These abnormalities, which were similar to those seen in human preeclampsia, included endothelial cell swelling, focal reduplication of the basement membrane, and fusion of the epithelial cell foot processes. The toxemia could not be attributed to changes in hematocrit, plasma glucose, Na, Cl, CO(2), K, Ca, fibrinogen, arterial pH, lactate, or pyruvate concentrations. Cardiac output fell only in ewes with prominent neurological signs. Plasma renin rose strikingly in animals developing toxemia, without change in substrate concentration. In contrast to human and other species, sheep uterus and amniotic fluid contained no detectable quantities of renin. Thus in response to stress the pregnant ewe develops a toxemia which in the absence of hypertension has clinical and pathological similarities to human preeclampsia.
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PMID:Toxemia of pregnancy in sheep: a clinical, physiological, and pathological study. 538 29

106 rabbits received one or more courses of inoculations, spaced 1-4 months apart, with Group A streptococci, usually of strains isolated from patients with acute glomerulonephritis. 8 days to a few weeks after onset of a given infection with streptococci known to have been nephritogenic for man, marked proteinuria, often with hematuria and occasionally with azotemia, was detected in 22 of the animals. 15 of these were sacrificed a few days to a few weeks thereafter, and 10 showed renal changes like those of acute or recurrent acute glomerulonephritis in man. Such changes occurred in three other rabbits whose urine was not examined that died or were sacrificed 1-3 wk after onset of infection with streptococci of a serotype known to include a strain nephritogenic for man. The remaining seven animals in which marked proteinuria had occurred died or were sacrificed many months later, in some cases after additional infections. Two of these had become azotemic and two convulsed and died after giving birth; in these animals, there were renal changes like those that occur in man in chronic latent glomerulonephritis, toxemia of pregnancy super-imposed on chronic latent glomerulonephritis, or chronic active glomerulonephritis. Anatomical changes in the kidneys in the experimentally induced and in naturally occurring glomerulonephritis, from acute to chronic stages, are compared and illustrated. The pathogenesis of poststreptococcal glomerulonephritis is discussed.
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PMID:The experimental induction of glomerulonephritis like that in man by infection with group A streptococci. 563 39

Hypertension may occur during pregnancy under different clinical circumstances. One cause is toxemia, a systemic disease unique to pregnant women, in which hypertension is associated with proteinuria, CNS irritability, hepatic and renal functional abnormalities, and, in fulminant disease, a consumptive coagulopathy. Since it is clear in the non-pregnant population that the vascular complications of hypertension can be prevented with antihypertensive therapy and since toxemia is the most common cause of maternal mortality, there is no reason not to treat pregnant women with hypertension.
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PMID:How should hypertension during pregnancy be managed? An internist's approach. 636 37

A new method is described for the preparation of highly purified human plasminogen and plasmin with specific activity of 32 CTA units per mg of protein. With this method, the purification of the urinary plasminogen + plasmin antigenic materials from patients with chronic glomerulonephritis, disseminated intravascular coagulation syndrome and severe toxemia of pregnancy was performed, and the resulting highly purified proenzyme and enzyme were analyzed by immunoelectrophoresis, separative agar electrophoresis, gel filtration and SDS-gel electrophoresis. Our findings indicated that urinary plasmin reflects more closely the extent of intraglomerular fibrinolysis, while urinary plasminogen reflects non-selective proteinuria in patients with chronic glomerulonephritis or severe toxemia of pregnancy.
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PMID:Studies on the purification and characterization of human urinary plasminogen and plasmin. 644 89

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

This communication describes the light, electron, and immunofluorescence microscopy of renal biopsy specimens from a patient with hydatidiform degeneration of the placenta and coexisting fetus. Symptoms of toxemia appeared in the 18th week of gestation and were accompanied by heavy proteinuria, decreased renal function, and disproportionately elevated serum uric acid concentration. The biopsy findings were consistent with the renal lesions of toxemia of pregnancy, although other renal diseases such as Henoch Schonlein nephritis or lupus proliferative glomerulonephritis cannot be excluded. Normal serological tests and disappearance of proteinuria, along with recovery of renal function to normal promptly after termination of pregnancy, tend to rule out other renal diseases. The molar transformation of the placenta, or the interaction with the kidney of certain humoral factors such as human chorionic gonadotropin which was markedly elevated in this patient, may be related to the pathophysiology of toxemia of pregnancy.
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PMID:Toxemic renal disease in incomplete molar pregnancy. 704 59


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