Behaviour Of Exogenous Heparin In Patients With Nephrotic Syndrome

1981 ◽  
Author(s):  
A M Fischer ◽  
M Guillot ◽  
R Girot ◽  
M Léon ◽  
P Triadou ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Antithrombin Iii ◽  
Thrombin Time ◽  
Control Groups ◽  
Blood Samples ◽  
Hemostatic System ◽  
Α2 Macroglobulin ◽  
Healthy Control ◽  
Nephrotic Children ◽  
Plasma Heparin

Behaviour of exogenous heparin was studied in 35 subjects after intravenous injection of 50 u/kg heparin : 10 healthy control adults, 8 control children with normal hemostatic system, 17 children with nephrotic syndrome without renal insufficiency. Blood samples were collected before injection and 15 min, 30 min, 60 min and 120 min later, for the following tests : APTT, thrombin time, automatised heparin assay using a chromogenic substrate (S-2238). Heparin behaviour was assessed by two criteria : recovery (plasma heparin level) 15 min after the injection ; halflife of recovered heparin. Results were compared with the following parameters : WBC and platelet count ; serum albumin and lipids ; plasma antithrombin III, α2 macroglobulin and fibrinogen ; histological findings when availableIn nephrotic children, mean heparin recovery was lower than in the control groups, very poor or even negligible in 9/17 cases. Heparin halflife was close to 37 min in most patients, shorter than in healthy controls (mean : 46 min), and dramatically decreased in 4 cases.No significant correlation was observed between the observed heparin behaviour and the considered parameters ; sensitivity to heparin was notably unrelated to plasma antithrombin III level. Insensitivity was observed in three patients with amyloidosis.

Comparison of Progressive Antithrombin Activity and the Concentration of Three Thrombin Inhibitors in Nephrotic Syndrome

1981 ◽  
Vol 46 (03) ◽  
pp. 623-625 ◽  
Author(s):  
B Boneu ◽  
F Bouissou ◽  
M Abbal ◽  
P Sie ◽  
C Caranobe ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Antithrombin Iii ◽  
Heparin Therapy ◽  
Thrombin Inhibitors ◽  
Compensatory Mechanism ◽  
Dramatic Reduction ◽  
Antithrombin Activity ◽  
Α2 Macroglobulin ◽  
At Iii ◽  
A Prospective Study

SummaryIn order to compare the plasmatic progressive antithrombin activity to the concentration of three thrombin inhibitors, antithrombin III (AT III), α2 macroglobulin (α2, M), α1 anti-trypsin (α1 AT) in nephrotic syndrome, a prospective study was carried out on a group of 28 children affected with the disease. A dramatic reduction of the level of AT III and of α1 AT, two inhibitors of molecular weight close to that of albumin, was observed. The decreased level of AT III was counterbalanced by an increase in α2 M. This phenomenon accounts for the increased progressive antithrombin activity observed in all the affected children. It is suggested that the above compensatory mechanism explains the absence of thrombotic accidents in this series and that the benefit of heparin therapy is doubtful in these conditions.

Modification of an Amidolytic Heparin Assay to Express Protein-Bound Heparin and to Correct for the Effect of Antithrombin III Concentration

1987 ◽  
Vol 58 (03) ◽  
pp. 884-887 ◽  
Author(s):  
Sandra G Lyon ◽  
Elliott C Lasser ◽  
Rosalyn Stein
Keyword(s):  
Molecular Weight ◽  
Dextran Sulfate ◽  
Antithrombin Iii ◽  
Low Molecular Weight ◽  
Accurate Assessment ◽  
Blood Samples ◽  
Concurrent Control ◽  
At Iii ◽  
Antithrombin Iii Concentration ◽  
Plasma Heparin

SummaryA modification of an anti-Xa assay for plasma heparin has been devised using a low molecular weight dextran sulfate that competitively binds protein heparin neutralizers and displaces masked heparin. The addition of 0.12 mg dextran sulfate per ml of plasma permits heparin, neutralized by the products of platelet aggregation, to recover full functional activity against Xa. The assay will permit a more accurate assessment of both exogenous plasma heparin and endogenous liepaiin-like activity in blood samples collected with varying techniques. A further modification is proposed employing polybrene to neutralize the plasma heparin-like material providing a concurrent control for each sample that increases accuracy by eliminating the effect of varying AT-III levels which have anti-Xa activity.

The Reversible Antithrombin Activity of Incubated Plasma

1977 ◽  
Vol 37 (01) ◽  
pp. 123-135 ◽  
Author(s):  
E. D Gomperts ◽  
J. C Stavridis ◽  
R. S Mibashan
Keyword(s):  
Calcium Ions ◽  
Antithrombin Iii ◽  
Thrombin Time ◽  
Platelet Poor Plasma ◽  
Antithrombin Activity ◽  
Physicochemical Changes ◽  
Enhanced Activity ◽  
Α2 Macroglobulin ◽  
Glass Tubes ◽  
Fibrin Monomers

SummaryThe thrombin time of normal citrated plasma is progressively prolonged on incubation in open glass tubes at 37° C. The phenomenon is dependent on the temperature and duration of incubation, on the pH, and on the concentration of calcium ions present. Platelet-rich citrated plasma fails to exhibit augmented antithrombin activity when similarly incubated, and the addition of washed platelets to platelet-poor plasma inhibits this activity. The clot retarding action of incubated plasma against thrombin is also manifested against Arvin (Ancrod), but not against Reptilase-R. This thrombin time lenghening may be inhibited by incubation with anti-antithrombin III antiserum thus indicating that the phenomenon of thrombin time lengthening is consistent with enhanced activity of antithrombin III. It is unlikely that alterations in the activity of α2-macroglobulin, is important in the reduced thrombin-coagulability of incubated plasma. Interference with the polymerisation of fibrin monomers by the physicochemical changes may contribute to the observed phenomenon.

Inhalation of Heparin and its Effect on Blood Coagulation

1979 ◽  
Author(s):  
M. Hellgren ◽  
K. Hägnevik ◽  
M. Blombäck
Keyword(s):  
Dose Group ◽  
Antithrombin Iii ◽  
Control Group ◽  
High Dose ◽  
Thrombin Time ◽  
Heparin Group ◽  
Blood Samples ◽  
Mean Values ◽  
Heparin Concentration ◽  
Observation Period

Heparin was administered by aerosol inhalation in principle according to Jaques et al. to 13 volunteers. The effects were investigated with activated partial thromboplastin tune (APT-time), thrombin-time and antithrombin III (Odegaard. Heparin concentration was measured in plasma according to Teien et al. and platelets were counted. Four volunteers received 700-800 IU heparin and 9, 1300 IU/kg b.w. Blood samples were drawn before, after and once a day for 10 to 21 days. Controls inhaled normal saline and blood samples were drawn for 12 days. No untowards effects were noted either on the day of inhalation or during observation period.On the day of inhalation heparin concentration in plasma increased in the heparin-group but not in the control group. A maintained level of heparin was measured up to 3 weeks afterwards in 9 of the 13 volunteers. The heparin concentrations increased fren mean values of 0.014 IU/ml plasma to a maximal mean value of 0.040 IU/ml plasma in the high dose and 0.039 IU/ml plasma in the low dose group. During the observation period heparin mean level was about 0.020 to 0.030 lu/ml plasma in the heparin group. In the control troup there was no measurable heparin. The APT and thrombin times were prolonged during the day of inhalation in the high-dose but not in the lew-dose group. Antithrombin III and ptc remained unchanged in both groups and no changes were noted in the control group.

scholarly journals Familial Primary Fibrinolysis

1977 ◽  
Author(s):  
Z. Currimbhoy
Keyword(s):  
Birth Control ◽  
Antithrombin Iii ◽  
Clot Lysis ◽  
Thrombin Time ◽  
Maternal Grandmother ◽  
Clotting Factors ◽  
Fibrin Plate ◽  
Α2 Macroglobulin ◽  
Birth Control Pills ◽  
Work Up

This study reports on a unique family with primary fibrinolysis. A 31-year-old female had hematuria of one month’s duration. She had a previous episode of hematuria lasting 3 weeks and a hysterectomy for menorrhagia. Her 10-year-old daughter bled from the gums at the age of 9 months for one week. All clotting factors (including Factors VIII, V and XIII) were normal, except Fibrinogen. The mother’s Fibrinogen varied from 110 to 165 mg%, and the daughter’s from 90 to 146 mg%. The diluted Thrombin Time and Reptilase times were normal. The most striking and constant defect was in the fibrinolytic system. These studies were performed over a 4 month period. Euglobulin clot lysis, done on the mother repeatedly and on the daughter twice, were abnormally short, varying from 60 to 100 minutes, with FSP>10 and <40 ug/ml or <10 ug/ml. Active lysis was present on fibrin plates. α2 macroglobulin, α1 antitrypsin and Antithrombin III were normal, as was plasminogen immunologically. Platelet count and functions were normal. The maternal grandmother bled profusely twice after two gynecological procedures and once needed a blood transfusion. She was then put on birth control pills. Work-up on the pill revealed a Fibrinogen of 217 mg%, but no clot formed when attempting to evaluate euglobulin lysis. Off the pill, Fibrinogen was 167 mg%, euglobulin clot lysis 30 mins,, and there was a zone of lysis on the fibrin plate.The congenital loss of an inhibitor to plasminogen activator could explain these results.

scholarly journals THE PATHOGENETIC SIGNIFICANCE OF HEMOSTASIS DISORDERS DETECTION FOR THE DIAGNOSTICS AND PREVENTION OF THROMBOTIC COMPLICATIONS IN WOMEN WITH ANTENATAL FETAL DEATH

2019 ◽  
Vol 111 (3) ◽  
pp. 21-28
Author(s):  
Antonina Kotenok ◽  
Nazariy Hychka ◽  
Vasyіl Beniuk
Keyword(s):  
Pregnant Women ◽  
Fetal Death ◽  
Antithrombin Iii ◽  
Fetal Loss ◽  
The State ◽  
The Body ◽  
Reproductive Age ◽  
Thrombin Time ◽  
Case Histories ◽  
Hemostatic System

The article summarizes the arguments and counterarguments within the scientific debate on the diagnosis and prevention of disorders in hemostatic blood system in women with antenatal fetal death. The main purpose of this investigation is to study the changes in the hemostatic system in pregnant women with antenatal fetal death, namely to evaluate the features of procoagulant, anticoagulant and fibrinolytic units of the hemostatic system in women with antenatal fetal death. The systematization of literary sources and approaches to the problem of hemostatic disorders in antenatal fetal death provides an opportunity to confirm the importance of this issue, to reasonably evaluate the risks during pregnancy in each particular woman and, first of all, to prevent the occurrence of this complication. This article presents the results of a retrospective study of individual case histories of pregnant women and the case histories of childbirth of women with antenatal fetal death and physiological pregnancy in the period from 2016 to 2018. The relevance of the study of this pathology is that every fifth woman of reproductive age faces a problem such as perinatal loss. In the structure of perinatal losses, antenatal fetal death occupies a special place, which can lead to the development of fetal loss syndrome, DIC, infectious complications in the mother and infertility or subfertility in the future, which in general has a negative impact on the reproductive potential of the nation. In the course of our work we evaluated such coagulogram indicators as: prothrombin index, thrombin time, activated partial thrombin time, soluble fibrin monomer complexes, plasma fibrinogen, antithrombin III, and protein C. It is established that pregnant women with antenatal fetal death are characterized by increased blood clotting activity against the background of suppression of anticoagulant and fibrinolytic units of hemostasis. Determination of the activity of antithrombin III informs about the state of anticoagulation system of the body and provides an opportunity to adjust the treatment with anticoagulant drugs of direct action. Indicators of coagulogram canʼt fully reflect the state of hemostasis during pregnancy, so the search for new methods of early diagnosis of imbalance in the system of hemostasis during pregnancy remains relevant at this stage. These studies may be useful for gynecologists, especially in women's counseling, for the formation of risk groups for pregnant women and for preventive measures to prevent antenatal fetal death.

Coagulation Studies in 45 Cases of Nephrotic Syndrome without Uremia

1970 ◽  
Vol 24 (03/04) ◽  
pp. 562-571 ◽  
Author(s):  
A Kanfer ◽  
D Kleinknecht ◽  
M Broyer ◽  
F Josso
Keyword(s):  
Nephrotic Syndrome ◽  
Factor Viii ◽  
Antithrombin Iii ◽  
Factor V ◽  
Thrombin Time ◽  
Thrombotic Complications ◽  
Eventual Death

SummaryCoagulation studies were performed in 45 cases of nephrotic syndrome without uremia. The most striking features were an increase in the number of thrombocytes, and in the level of fibrinogen, factor V and factor VIII. Thrombin time was usually prolonged and the titre of antithrombin III was increased. No fibrin breakdown products were found in the serum. 13 patients developed thrombotic complications, with eventual death in 5 cases.

Dysfibrinogenemia and Hypercoagulability in Patients with Membranous Glomerulopathy

1979 ◽  
Author(s):  
C. S. Winter ◽  
R. D. Wagoner ◽  
E. J. W. Bowie ◽  
C. A. Owen
Keyword(s):  
Nephrotic Syndrome ◽  
Renal Vein ◽  
Antithrombin Iii ◽  
Degradation Products ◽  
Renal Vein Thrombosis ◽  
Thrombin Time ◽  
Vein Thrombosis ◽  
Membranous Glomerulopathy ◽  
Normal Mean ◽  
Fibrinogen Molecule

Renal vein thrombosis (RVT) is a common complication in patients with nephrotic syndrome and membranous glomerulopathy (MGN). We demonstrated it angiographically in 12 of 24 consecutive patients. Thorough hemostatic surveys were done on 14, 6 with RVT. In 11 patients, 5 with RVT, platelet counts were significantly above normal, 402,000 to 700,000/mm3 blood. In all but 4 cases, plasma fibrinogen was at least twice normal (mean 588 mg/dl). Factor VIII: C levels ranged from 152 to 337 U/dl (mean 236). Antithrombin III was depressed in only one patient, lie did not have RVT. While prothrombin times, partial thromboplastin times, and activated partial thromboplastin times were normal in all patients (except when anticoagulants were being given), the thrombin time was significantly prolonged in 12 of the 14 patients (6 with RVT). In these 12 the Reptilase times were also long. The prolonged thrombin times cannot be attributed to inhibition by fibrinolytic degradation products since the FDP were elevated in only 5 cases (2 with RVT). It seems that an abnormality of the fibrinogen molecule (prolonged thrombin and Reptilase times) and “hypercoagulability” characterize the nephrotic syndrome associated with membranous glomerulopathy and possibly other renal lesions. We could not, however, distinguish between patients with and without renal vein thrombosis.

Inherited Antithrombin Deficiency Causing Thrombophilia

1965 ◽  
Vol 13 (02) ◽  
pp. 516-530 ◽  
Author(s):  
O Egeberg
Keyword(s):  
Autosomal Dominant ◽  
Antithrombin Iii ◽  
Thrombin Time ◽  
Dominant Trait ◽  
Autosomal Dominant Trait ◽  
Antithrombin Deficiency ◽  
Heparin Resistance ◽  
High Incidence ◽  
History Of ◽  
Plasma Heparin

SummaryBlood coagulation systems were studied in members of a family with remarkably high incidence of thrombo - embolic diseases. Thrombotic episodes most often occurred as deep venous thrombosis in the legs, with the first attack at the age of 10-25 years.Pro coagulant factor activities were found within normal variation ranges.Plasma antithrombin III (progressive antithrombin) activity was abnormally low in members with history of thrombosis and in some of their children, with an average level of about 50 per cent of normal.Heparin resistance measured with plasma heparin thrombin time was increased in members with low antithrombin III, and plasma heparin cofactor activity was decreased.The results strongly support the explanation that antithrombin III and heparin cofactor are one and the same plasma substance, and that deficiency of this antithrombin can cause a severe tendency to thrombosis.The antithrombin deficiency seems to be inherited as an autosomal dominant trait.

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