Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Masugi nephritis was induced in dogs in which platelet count, fibrinogen, antithrombin activity, plasma prekallikrein and immediate plasmin inhibitors were coincidentally decreased immediately after the injection of nephrotoxin serum. It was found that the grade of decrease of urinary kallikrein excretion following these immediate reactions were parallel with the grade of renal damages. By the pretreatment with heparin or the defibrination with snake venom, however, the histological findings of Masugi nephritis showed rather severe damage. Based on the consumption of coagulation factors, kallikrein, kinin and their inhibitors in the development of this nephritis, it was postulated that inauguration of coagulation and activation of kallikrein contributed to the development of glomerulonephritis. The treatment or prevention of this coagulation process with heparin or snake venom, however, gave untoward effects on the pathological process in this experiment.
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PMID:Participation of kallikrein, coagulation/fibrinolysis parameters in the development of glomerulonephritis. 49 36

Human plasma prekallikrein (Fletcher factor) clotting activity and antigen levels have been examined in various clinical conditions. Prekallikrein antigen was measured by a newly developed, specific, and sensitive radioimmunoassay. The assay had no demonstrable cross-reactivity with human urinary kallikrein nor, in the species tested, animal plasma prekallikrein. This assay was able to measure plasma kallikrein after its biological functions had been inactivated by plasma inhibitors. Normal human pooled plasma contained approximately 50 microgram/ml prekallikrein. Quantitative measurement of plasma prekallikrein was possible for concentrations as low as 0.3% of that of normal pooled plasma. A good correlation (correlation coefficient = 0.71) existed between titers of plasma prekallikrein measured by Fletcher factor clotting assays and radioimmunoassays among 40 normal subjects. Both prekallikrein clotting activity and antigen were significantly reduced in plasmas of patients with advanced hepatic cirrhosis or DIC. Prekallikrein activity and antigen were mildly decreased in plasmas or serums of patients with chronic renal failure and nephrotic syndrome but were normal in those of patients under treatment with warfarin or suffering from SLE, rheumatoid arthritis, sarcoidosis, or HANE. Human cord serum contained a lower titer of prekallikrein antigen than adult serum. Strenuous physical exercise did not significantly change plasma prekallikrein levels.
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PMID:Human plasma prekallikrein (Fletcher factor) clotting activity and antigen in health and disease. 65 66

To investigate the role plasma kallikrein plays in the in vivo activation of inactive renin, we measured plasma active renin, inactive renin, kallikrein and prekallikrein levels in 10 patients with disseminated intravascular coagulation (DIC), with 16 normal persons as controls. The plasma active renin concentration was expressed by the angiotensin I generation rate after the addition of sheep renin substrate. Plasma inactive renin was activated by trypsin. The plasma total kallikrein level was measured by an assay of kallikrein activity on synthetic substrate S-2302 after the addition of a prekallikrein activator. Plasma kallikrein was assayed by its activity on S-2302 without addition of the activator. The prekallikrein level was obtained by subtracting the kallikrein activity from the total kallikrein activity. A significant decrease in the plasma prekallikrein concentration was observed in DIC patients, as compared to that of controls (p less than 0.01). There was no significant difference in plasma levels of kallikrein, inactive renin, and the proportion of active renin between DIC patients and normal controls, but the active renin level was higher in DIC patients. There was no significant correlation between the level of plasma kallikrein and the proportion of active renin in either normal controls or DIC patients. These results are compatible with, but do not prove, the theory that plasma kallikrein plays a role in the in vivo activation of inactive renin.
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PMID:Plasma active renin, inactive renin and kallikrein in patients with disseminated intravascular coagulation. 168 Sep 81

We studied contact factors and kinin-kallikrein in normal non-pregnant and pregnant women, FXII deficient toxemia and DIC. The results obtained are as follows: 1. The levels of plasma prekallikrein, high molecular weight kininogen, kallikrein inhibitor, and C-1 INA were gradually decreased at delivery, and the levels of kallikrein like activity and bradykinin were increased during pregnancy and at the time of parturition. These facts indicate that kinin kallikrein systems played important role in uterine contraction. 2. The levels of contact factors (FXII and FXI) were lower at delivery than those of term. 3. In rat uterus, specific binding of bradykinin was observed by the method of radio receptor assay in the pelet of 10,000 X g fetal membranes, and its activity was 38%. 4. A synthetic kallikrein inhibitor (OS-291, MS) and bradykinin antagonist inhibited completely spontaneous uterine contraction of Wistar rats during delivery. 5. In the case of FXII deficiency, the levels of plasma prekallikrein, high molecular weight kininogen were normal, but at delivery, these levels were lower than those of term. The levels of kallikrein like activity which was half of normal parturition level was increased at parturition. 6. In cases of DIC (17) and severe toxemia (22), plasma prekallikrein levels were lower than the normal controls. The decrease was due to consumption of plasma prekallikrein to kallikrein activation.
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PMID:[Physiopathology of kinin forming system in reproduction]. 259 38

Plasma kallikrein acts as a chemical mediator of microcirculation and as a contracting agent of smooth muscle by liberating bradykinin from high molecular weight kininogen. In addition, prekallikrein relates to coagulation process of blood. It is, therefore, a intriguous problem to know the behavior of prekallikrein in obstetrics, especially as to the mechanisms of labor, edema of toxemia and DIC. The following results were obtained: 1) Plasma prekallikrein determined by chromogenic tripeptide substrate was increased with advance of gestational ages, and reached maximum (213.5 +/- 31.1%) at the term. At the beginning of labor, the prekallikrein level was suddenly decreased, and remained low during labor. Rapidly lowered plasma prekallikrein during labor seems to be result from consumption of prekallikrein due to conversion to kallikrein. The kallikrein probably relates to uterine contraction by forming bradykinin. 2) A lowered plasma prekallikrein level was observed in 29 cases of toxemia, especially in edema type. In toxemic cases, kallikrein may play an important role in producing edema by bradykinin. 3) In 16 cases of DIC, prekallikrein was significantly low (p less than 0.001) especially in cases of endotoxic shock, suggesting consumption of prekallikrein as in other various coagulation fibrinolysis factors in DIC.
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PMID:[Physiological and pathological significance of plasma prekallikrein in obstetrics]. 692 84