scholarly journals Antithrombin III and fibrinogen degradation product (fragment E) in diabetic nephropathy.

1982 ◽  
Vol 35 (6) ◽  
pp. 661-666 ◽  
Author(s):  
V Chan ◽  
C K Yeung ◽  
T K Chan
1977 ◽  
Vol 38 (02) ◽  
pp. 0494-0503 ◽  
Author(s):  
D. S Pepper ◽  
D Banhegyi ◽  
J. D Cash

SummaryAntithrombin III (AT III) complexes were isolated from human serum by affinity chromatography and gel filtration. In the first step of the preparation, using heparin-agarose chromatography, we observed that the complexed form of AT III bound less strongly to the gel than the free form and that about half of the AT III was free. With further purification a 2.5 × 105 molecular weight complex was isolated. Using 125I labelled human thrombin, this complex was radioactive indicating the presence of thrombin. Only in a synthetic thrombin-AT III system was a 9 × 104 molecular weight complex detected, but not in serum. These facts suggest that in serum AT III complexes may exist in a polymeric form. Also, an AT III antigen derived from the original AT III molecule, but not complexed, was isolated which may be a degradation product.Abbreviations used: AT-III, antithrombin III. Hepes, N-2-Hydroxyethylpiperazine-N-2-Ethanesulphonic acid.


1981 ◽  
Author(s):  
Vivian Chan ◽  
C K Yeung ◽  
T K Chan

We measured plasma and urine ATIII and FgE levels by specific and sensitive radioimmunoassays (RIA) in 25 patients with diabetic nephropathy (DN) (proteinuria > lg/day) and in 17 patients with non-diabetic glomerulonephritis (GN), matched for degree of proteinuria. Plasma ATIII in DN (mean ± SD, 19.37 ± 2.40 mg/dl) were lower than in diabetics without renal involvement (21.84 ± 2.86 mg/dl). Total urine ATIII was directly related to proteinuria and inversely to creatinine clearance. In GN patients, plasma ATIII levels were even lower (16.84 ± 3.78 mg/dl), but the amount of urine ATIII fell when creatinine clearance decreased to below 37 ml/min. Serum FgE levels were elevated in both groups and this was associated with increased total urine FgE excretion. In DN, serum and urine FgE were directly related to proteinuria but inversely to creatinine clearance, indicating an increase in intraglomerular fibrin deposition as the disease progressed. These findings suggest that in DN, intravascular thrombosis might play an intermediary role as mediator of glomerular injury. Furthermore, the monitor of urine ATIII and FgE reflected the severity of DN and could be useful indices of the progression of the disease.


1981 ◽  
Vol 55 (5) ◽  
pp. 718-724 ◽  
Author(s):  
J. Jaap van der Sande ◽  
Jan J. Veltkamp ◽  
Ria J. Boekhout-Mussert ◽  
G. Jan Vielvoye

✓ Coagulation studies (plasma fibrinogen, ethanol gelation test, and fibrin-fibrinogen degradation product concentration) and computerized tomography (CT) scan examinations were performed in 55 patients with blunt head injury. The frequency of abnormalities in both coagulation study results and CT scans was higher in patients with severe clinical features and clinical course than in less severely injured patients; in these same patients the coagulation results were abnormal (64%) more frequently than the CT scans (40%). Very high fibrin-fibrinogen degradation product (FDP) concentrations were found to be associated with combined hemorrhagic lesions and mass effect on CT scans, but not with a specific localization of braintissue damage. It was concluded that: 1) FDP concentration reflects the amount of brain-tissue damage rather than its location, and 2) in the absence of other possible causes of disseminated intravascular coagulation, coagulation studies may be more sensitive than CT scanning in demonstrating brain contusion.


1983 ◽  
Vol 58 (5) ◽  
pp. 693-698 ◽  
Author(s):  
J. Jaap van der Sande ◽  
Jan J. Veltkamp ◽  
Marijke L. Bouwhuis-Hoogerwerf

✓ Preoperative and postoperative coagulation studies were performed in 25 patients undergoing various intracranial surgical procedures. Coagulation abnormalities, mostly consisting of an increase of fibrin/fibrinogen degradation product concentration, either appeared or increased postoperatively in 18 patients. This incidence of postoperative appearance or increase of coagulation abnormalities is higher than that reported in a comparable study of patients after general surgical procedures, and also higher than that of coagulation abnormalities in a previous study of patients after blunt head injury. Although the coagulation abnormalities after intracranial surgery were usually small, they tended to be larger in patients with more extensive intracranial procedures.


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