Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coagulation studies were done on 78 consecutive cases of obstructive jaundice with or without biliary tract infection. Among 26 cases with biliary tract infection 20 cases showed no bleeding tendency but remarkable hypercoagulability with decreased fibrinolytic activity. Other six cases developed diffuse bleeding tendency in addition to the signs of hypotension and multiorgan dysfunction such as oliguria, respiratory distress and mental confusion. Most showed marked coagulation defects characterized by thrombocytopenia, decreased fibrinogen, antithrombin III and plasminogen levels and narrowing of maximal amplitude in thrombelastogram as well as the increase of fibrin degradation products and positive soluble fibrin monomer complexes. All except one died and three cases were autopsied. In two cases postmortem examination revealed multiple fibrin thrombi in lungs and other organs. A cause of the development of bleeding tendency in obstructive jaundice presently observed may likely to be due to the occurrence of disseminated intravascular coagulation (DIC), i.e. hypercoagulability caused by the biliary tract infection is responsible.
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PMID:Occurrence of disseminated intravascular coagulation (DIC) in obstructive jaundice and its relation to biliary tract infection. 32 28

Burn injury causes dynamic alterations in the coagulation and fibrinolysis, and so-called DIC often occurs in burned patients. In this study the clinical significance of heparin therapy combined with antithrombin III concentrate in animal experiments and clinical experiences were discussed. The changes in blood coagulation, fibrinolysis and kidney function and the effect of anticoagulation therapy using heparin were investigated in rabbits with third degree burn covering 35% of the total body surface area. The animals were subjected to determinations for various kidney function tests, blood coagulation and fibrinolysis tests, blood viscosity and hematocrit value before induction of the burn and after 8 and 24 hours respectively. Thirty rabbits were divided into a non-therapy group, an intravenous infusion group, a heparin group, an antithrombin III group, and an antithrombin III plus heparin group and the results were compared among them. Oliguria and a disturbance of kidney function were noted even at hour 8 after burn in the non-therapy group. In the intravenous infusion group urine volume was maintained well although the early stage of non-oliguric renal insufficiency was noted. The changes noted in the intravenous infusion group were prevented almost completely in the heparin group at hour 8, but FENa and CH2O were elevated at hour 24 probably because antithrombin III activity was depressed markedly. In the antithrombin III group and the antithrombin III plus heparin group, however, creatinine clearance was moderately elevated while FENa and CH2O remained unchanged as compared with the values before the burn. The antithrombin III plus heparin group showed slightly better results than the antithrombin III group in Ucr/Pcr ratio, creatinine clearance and CH2O. The results of the present study indicate that it is extremely effective to initiate appropriate fluid infusion therapy immediately after a burn and administer antithrombin III concentrate in combination with or without heparin for the prevention of acute renal insufficiency in patient with a severe burn. The effects of antithrombin III concentrate when used clinically were also discussed.
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PMID:[Alteration in coagulation and fibrinolysis after burn injury and significance of anticoagulation therapy using heparin and antithrombin III concentrate]. 381 36

The changes in blood coagulation, fibrinolysis and kidney function and the effect of anticoagulation therapy using herapin were investigated in rabbits with full thickness skin loss burns covering 35 per cent of the total body surface area. Determinations of various kidney function tests, blood coagulation and fibrinolysis tests, blood viscosity and haematocrit values were made before burning and after 8 and 24h. Thirty rabbits were divided into a non-therapy group, an intravenous infusion group, a heparin group, an antithrombin III group and an antithrombin III plus heparin group and the results were compared. Oliguria and a disturbance of kidney function were noted 8 h after the burn in the non-therapy group. In the intravenous infusion group urine volume was well maintained although the early stage of non-oliguric renal insufficiency was noted. The changes noted in the intravenous infusion group were prevented almost completely in the heparin group but FENa and CH2O were elevated at 24h probably because antithrombin III activity was markedly depressed. In the antithrombin III group and the antithrombin III plus heparin group, however, creatinine clearance (Clcr) was moderately elevated while FENa and CH2O remained unchanged as compared with the values before the burn. The antithrombin III plus heparin group showed slightly better results than the antithrombin III group in Ucr/Pcr ratio, Clcr and CH2O. The results of the present study indicate that it is extremely effective to initiate appropriate fluid therapy immediately after a burn and to administer antithrombin III concentrate in combination with or without heparin for the prevention of acute renal insufficiency in patients with a severe burn.
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PMID:Anticoagulation therapy for renal insufficiency after burns. 652 33

Willebrand's factor (WF), antithrombin III (AT-III), blood 5'-nucleotidase and athrombogenic properties of the vascular wall were studied in the course of the disease in 69 patients suffering from hemorrhagic fever with renal syndrome (HFRS). The patients were chiefly under 27 years, had severe or moderate condition. It was found that WF rose 3-fold in oliguria, but returned to normal values by convalescence. AT-III remained stable. High activity of 5'-nucleotidase reached the pick in oliguria and polyuria. As shown by a cuff test, athrombogenic potential of the vascular wall remained low. A role of vascular endothelial impairment in HFRS is discussed.
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PMID:[Von Willebrand factor, antithrombin III and 5'-nucleotidase in the blood and the athrombogenic properties of the vascular wall in patients with hemorrhagic fever with renal syndrome]. 790 37

We tested the hypothesis that enhanced intravascular coagulation in pregnancy could produce clinical symptoms similar to those of preeclampsia, such as hypertension, proteinuria, and edema. Having confirmed this, we then examined whether the pathological changes caused by intravascular coagulation could be suppressed by administration of antithrombin III (AT III), an endogenous inhibitor active to thrombin and factor X a. Intravascular coagulation was induced in Wistar rats on day 16-20 of pregnancy by 1-h arterial infusion of tissue thromboplastin (TP) through the left ventricle of the heart. One hour after the end of the infusion period, organ blood flows were measured by the radioactive ((57)Co-labeled) microsphere method, and fibrin deposition in organs was measured by radiolabeling with [(125)I] fibrinogen injected before TP infusion. Infusion of TP produced fibrin deposition in the kidney, lung, and liver, but not in the myometrium and placenta, as well as an 80% decrease in renal blood flow (RBF), with oliguria and proteinuria. TP also caused an increase in blood pressure (BP) accompanied by an increase in plasma renin activity (PRA), both of which were suppressed by bilateral nephrectomy before TP infusion. The prophylactic administration of AT III concentrates (60 or 300 U/kg intravenously (i.v.), followed by infusion of 30 or 150 U/kg/2 h, respectively) prevented all pathological changes in a dose-dependent manner. AT III increased placental blood flow regardless of the state of coagulation. These findings suggest that intravascular coagulation plays a significant part in the pathophysiology of preeclampsia and that AT III concentrates may have therapeutic potential in the treatment of this condition.
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PMID:Antithrombin III prevents renal dysfunction and hypertension induced by enhanced intravascular coagulation in pregnant rats: pharmacological confirmation of the benefits of treatment with antithrombin III in preeclampsia. 885 41