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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical manifestations of severe pre-eclampsia are normally separated from those of mild pre-eclampsia and normal pregnancy on arbitrary grounds. A clinical index, based on the increase in diastolic blood-pressure and the presence of proteinuria, was developed to reflect the spectrum of disease from mild to severe pre-eclampsia. This was related to a coagulation index based on the platelet-count, plasma-factor-VIII, and serum-fibrinolytic-degradation-products. The two indices were shown to be strongly correlated. All cases of perinatal death associated with pre-eclampsia had coagulation indices in the most severely abnormal range. These results suggest that intravascular coagulation is a highly characteristic feature of pre-eclampsia and that the coagulation index may be of value in monitoring the progress of the disease.
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PMID:Use of coagulation tests to predict the clinical progress of pre-eclampsia. 6 May 64

Researchers analyzed data on 47 black, pregnant women of more than 33 weeks gestation who had preeclampsia with diastolic blood pressure of at least 110 mm Hg and 1+ of proteinuria and were in the delivery department of King Edward VIII Hospital in Durban, South Africa to compare antihypertensive effects of dihydralazine infusion with that of epoprostenol sodium infusion. Overall, both treatments reduced the patient's systolic and diastolic blood pressures. No significant differences in the hypertensive effects existed between the 2 groups. Yet the reduction in blood pressures occurred much more quickly in the epoprostenol group than in the dihydralazine group (51.1 minutes vs. 86.8 minutes;p=.0072). Epoprostenol reduced high blood pressure in all 22 patients while dihydralazine did not adequately control blood pressure in 2 of 25 patients. Physicians had to perform a cesarean section in these 2 cases due to considerable deceleration of the fetal heart rate. They had to 1st administer the rapidly acting ganglion blocking agent, trimetaphan, before placing the women under general anesthesia. Their blood pressures returned to normal after delivery. Even though both groups experienced tachycardia after treatment, the pulse rate of dihydralazine patients was significantly higher than that of epoprostenol patients (102.68/minute vs. 88.36/minute; p=.0024). Only 2 women suffered from side effects. The epoprostenol patient experienced nausea and vomiting. The other patient received dihydralazine and experienced a severe headache. The researchers concluded that physicians should use epoprostenol in patients with severe hypertension and tachycardia and those who need acute control of severe hypertension on the operating table before endotracheal intubation (which tends to cause considerable increases in blood pressure) and administration of general anesthesia.
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PMID:A comparative study of the use of epoprostenol and dihydralazine in severe hypertension in pregnancy. 142 10

Nephrotic syndrome (NS) is associated with several disorders of hemostasis: thrombocytosis and platelet hyperaggregability; increased plasma levels of factors V and VIII, and of fibrinogen with blood hyperviscosity; decreased plasma levels of natural anticoagulants: free protein S, and antithrombin III compensated by increased levels of alpha 2-macroglobulin; lowered fibrinolytic activity. Intensity of hypercoagulability is related to the degree of hypoalbuminemia; however, the role of hypercoagulability in the increased incidence of thromboembolic events, including renal vein thrombosis, is not proved. Clotting disorders are due to urinary losses of anticoagulants or to increased liver synthesis of procoagulants stimulated by hypoalbuminemia. Moreover, changes in clotting factors levels may be due to intravascular thrombin formation (marked by increased plasma levels of fibrinopeptide A). During active phases of glomerulonephritides (GN) with NS, thrombin formation might in fact arise in glomeruli, following activation of the glomerular hemostasis system. Isolated glomeruli from human crescentic GN, rabbit nephrotoxic GN and rat HgCl2 autoimmune GN produce excessive amounts of procoagulant (tissue factor) activity (PCA). Sequential studies of the self-limited HgCl2 GN showed that glomerular PCA, proteinuria and glomerular fibrin deposits peaked concomitantly at the acme of the disease, suggesting that immunologically mediated glomerular damage had triggered the extrinsic coagulation pathway.
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PMID:Coagulation factors in nephrotic syndrome. 225 77

A 4-year-old Japanese girl had a congenital disorder that was characterized by recurrent thrombocytopenia, hemolytic anemia, hematuria, and proteinuria, which were repeatedly improved by the infusion of factor VIII concentrate. She developed the similar symptoms within 1 h after 1-desamino-8-D-arginine vasopressin (DDAVP) administration. Coagulation studies 30 and 60 min after DDAVP infusion showed a disappearance of large factor VIII:von Willebrand factor (VIII:vWF) multimers, which was the same abnormality that was observed at acute episodes. There were no significant changes in the plasma levels of 6-keto-prostaglandin F1 alpha and thromboxane B2 before and after DDAVP infusion. These results provide further support that VIII:vWF is directly involved in the pathogenesis of this congenital disorder.
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PMID:Factor VIII concentrate-responsive thrombocytopenia, hemolytic anemia, and nephropathy. Evidence that factor VIII:von Willebrand factor is involved in its pathogenesis. 309 91

To investigate whether the elevation of factor VIII coagulant activity observed in children with poor control of diabetes is due to increased levels of the factor VIII coagulant moiety of the factor VIII complex or reflects activation of the factor VIII coagulant moiety, factor VIII coagulant activity (VIII C), factor VIII coagulant antigen (VIII C:Ag), and factor VIII-related antigen (VIII R:Ag) were determined in 75 insulin-dependent children. All children were without signs of vascular disease based on negative funduscopy, negative fluorescein angiography, normal serum creatinine levels, and absence of proteinuria. Children with poor actual control of diabetes had significantly higher VIII C values than did children with good actual control of diabetes based on HbA1 values, but VIII C:Ag values did not differ in children with good or poor actual control of diabetes. A significant elevation of VIII C over VIII C:Ag values was observed in children with poor actual control of diabetes, but no elevation of VIII C over VIII C:Ag was found in children with good actual control. VIII R:Ag values were higher in children with poor actual control. VIII C, VIII C:Ag, and VIII R:Ag did not differ significantly in children with short or long duration of clinical diabetes. Our observation of significantly higher VIII C values than VIII C:Ag levels strongly suggests intravascular activation of the factor VIII coagulant moiety during poor diabetes control. The process leading to activation of the coagulant moiety seems to be different from the process leading to the elevation of the other moiety of the factor VIII complex, the factor VIII-related antigen, in diabetic subjects.
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PMID:Elevation of Factor VIII coagulant activity over Factor VIII coagulant antigen in diabetic children without vascular disease. A sign of activation of the Factor VIII coagulant moiety during poor diabetes control. 391 55

This report describes a patient with thrombocytopenia, microangiopathic hemolytic anemia, proteinuria, and microscopic hematuria that could be transiently improved by the infusion of plasma or various plasma components. An increase in platelet count following the transfusion of normal plasma was predictable and reproducible. In therapeutic trials with commercially available plasma components, factor VIII preparations were effective for inducing an increase in the platelet count and improving hemolytic anemia, but albumin, gamma-globulin, factor IX, and fibronectin preparations were ineffective. Serum from normal donors also relieved the symptoms of this condition in our patient. Partial plasma exchange (1,000 ml/m2 of body surface area) was performed with albumin instead of normal plasma, but there was no significant effect on platelet count or anemia. Large, multimeric von Willebrand factor components of the factor VIII complex (VIII/vWF) were found in the patient's plasma when his platelet count was normal, but their levels were reduced when the platelet count was decreased. The multimers of the patient's plasma were larger than those in normal plasma, but smaller than those in normal platelet lysate. Although the pathogenesis of this disease remains unknown, we conclude that transfusions of normal plasma, serum or factor VIII concentrate provide a factor that causes significant improvement in the thrombocytopenia and hemolytic anemia. Furthermore, large VIII/vWF multimers are possibly directly involved in pathogenesis of this disease.
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PMID:Efficacy of several plasma components in a young boy with chronic thrombocytopenia and hemolytic anemia who responds repeatedly to normal plasma infusions. 643 3

A patient with clinical and laboratory evidence of von Willebrand syndrome is described in association with an IgG-kappa immunoglobulin and Bence-Jones proteinuria due to a probable lymphoproliferative disorder. He had a persistently prolonged bleeding time of greater than 20 minutes, factor VIII related antigen (VIII:R.Ag), factor VIII procoagulant activity (VIII:C) and factor VIII ristocetin co-factor (VIIIR:Rcof) below 10%. Following cryoprecipitate or high purity factor VIII concentrate infusion, he had the expected immediate rise in VIII:C, VIII:R.Ag, and VIIIR:Rcof, but there was a rapid decline in all three components within two hours. The larger forms of VIII:R.Ag were preferentially removed from the plasma, and this paralleled the fall in plasma VIIIR:Rcof level. However, no inhibitory activity could be demonstrated in vitro using the patient's plasma or IgG. Using protein A it was possible to demonstrate that his plasma or IgG bound factor VIII and that this complex retained its biological activity in vitro. It is postulated that the monoclonal IgG forms complexes with factor VIII in vivo and these are rapidly removed by the reticuloendothelial system (RES).
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PMID:Pathogenesis of antibody-induced acquired von Willebrand Syndrome. 678 64

Levels of factor VIII/von Willebrand factor were measured in 105 patients affected by glomerulonephritis either of primary origin or associated with systemic diseases. The median plasma concentration of factor VIII-related antigen was significantly higher in the patients than in healthy controls. Amongst patients with primary glomerulonephritis, higher levels were observed in minimal change nephropathy than in other types. In patients with secondary glomerulonephritis, plasma factor VIII-related antigen was particularly elevated in lupus nephritis and in renal amyloidosis. Altogether, patients with the nephrotic syndrome showed higher levels than patients with lesser degrees of proteinuria. A negative correlation was found between the plasma concentration of factor VIII-related antigen and that of serum albumin but no correlation was observed with the extent of proteinuria. In 48 patients, plasma factor-VIII procoagulant activity was also measured and found to be elevated to the same extent as factor VIII-related antigen in the majority of cases. The urinary excretion of factor VIII-related antigen, evaluated in 72 patients, was found in variable amounts in 31 cases without any correlation with proteinuria. Glomerular deposits of factor VIII-related antigen were an uncommon finding. After 24 months, there was no clear evidence of an unfavourable association between increased plasma levels of factor VIII-related antigen and the course of the disease. Our findings suggest that the measurement of levels of factor VIII/von Willebrand factor in plasma or urine must be interpreted with caution in predicting the clinical course of patients affected by glomerular disease.
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PMID:Factor VIII/von Willebrand factor in glomerular nephropathies. 679 18

Factor VIII coagulant activity (VIII C) and factor VIII-related antigen (VIII R:Ag) were studied in 86 insulin-dependent diabetic children. All children were without signs of vascular disease based on a negative funduscopy, negative fluorescein angiography, normal serum creatinine levels, and absence of proteinuria. Age ranged from 4 to 17 yr; duration of clinical diabetes ranged from 1 to 12 yr. The children were grouped according to their urinary sugar excretion, the HbA1 levels, and the duration of clinical diabetes. The group with high urinary sugar excretion and the group with high HbA1 levels had a significantly higher VIII C than the group with low urinary sugar excretion and the group with low HbA1 levels. VIII C levels did not differ significantly in the groups with a different duration of clinical diabetes, but VIII R:Ag was significantly higher in the group with the longest duration of diabetes as compared with the group with the shortest duration. VIII R:Ag levels did not differ significantly in the groups with different degrees of urinary sugar excretion or different HbA1 levels. The results show that in children without vascular disease, and even in children with a short duration of diabetes, alterations of the factor VIII complex can be demonstrated.
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PMID:Elevated factor VIII activity and factor VIII-related antigen in diabetic children without vascular disease. 681 42

During a survey of all pregnant patients seen during 1 month at the King Edward VIII Hospital, Durban, the prevalence of hypertension in pregnancy proved to be 11,4%. The incidence in primigravidas was 17,8%, twice the figure in multigravid patients. The perinatal mortality rate for both groups of patients was increased, especially when proteinuria was also present. The infants born to the multigravid patient with hypertension and proteinuria not only have a higher risk of perinatal mortality (5 - 6-fold increase) but a significantly lower birth weight than the infant born to the primiparous patient.
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PMID:A survey of hypertension in pregnancy at the King Edward VIII Hospital, Durban. 742 93


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