Antithrombin III and Heparin Cofactor II in Patients with Chronic Renal Failure Undergoing Regular Hemodialysis

1987 ◽  
Vol 57 (03) ◽  
pp. 263-268 ◽  
Author(s):  
P Toulon ◽  
C Jacquot ◽  
L Capron ◽  
M -O Frydman ◽  
D Vignon ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Plasma Proteins ◽  
Antithrombin Iii ◽  
Vascular Wall ◽  
Relative Increase ◽  
Heparin Cofactor Ii ◽  
Normal Ranges ◽  
At Iii ◽  
Regular Hemodialysis

SummaryHeparin enhances the inhibition rate of thrombin by both antithrombin III (AT III) and heparin cofactor II (HC II). We studied the activity of these two plasma proteins in patients with chronic renal failure (CRF) undergoing regular hemodialysis as their heparin requirements varied widely. In 77 normal blood donors, normal ranges (mean ± 2 SD) were 82-122% for AT III and 65-145% for HC II. When compared with these controls 82 dialyzed CRF patients had a subnormal AT III activity and a significantly (p <0.001) lower HC II activity. To evaluate the effect of hemodialysis we compared AT III, HC II and total proteins in plasma before and after dialysis in. 24 patients (12 with normal and 12 with low basal HC II activity). AT III and HC II activities significantly (p <0.001) increased in absolute value. When related to total plasma proteins, in order to suppress the influence of hemoconcentration induced by dialysis, AT III decreased significantly (p <0.01) whereas HC II increased slightly but significantly (p <0.01) in the 12 patients with low initial HC II activity. The decrease of AT III induced by heparin administrated during dialysis is likely to account for this relative decrease of AT III activity. A modification of the distribution of both HC II and heparin between the vascular wall and the circulating blood is evoked to explain the relative increase in HC II activity and the need for higher heparin dosage in patients with low HC II levels.

ANTITHROMBIN III AND HEPARIN COFACTOR II IN PATIENTS WITH CHRONIC RENAL FAILURE

1987 ◽  
Author(s):  
P Toulon ◽  
C Jacquot ◽  
M O Frydman ◽  
D Vignon ◽  
M Aiach
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Plasma Proteins ◽  
Blood Donors ◽  
Dermatan Sulfate ◽  
Control Group ◽  
Dialysis Session ◽  
Heparin Cofactor Ii ◽  
At Iii ◽  
Before And After

Anti thrombin III (AT III) and heparin cofactor II (HC II) were measured in 77 blood donors, 82 patients with chronic renal failure (CRF) undergoing regular hemodialysis and 36 undialyzed patients with CRF. AT III was measured as heparin cofactor and HC II as dermatan sulfate cofactor using amidolytic assays.The results (mean ± SD expressed in percentage of the in pooled normal plasma) are summurized in the table.Subnormal AT III levels were found in both dialyzed and undialyzed patients with CRF, while HC II was significantly (p < 0.001) reduced in dialyzed patients (12 of them were found to have HC II levels below to lowest value founded in our control group: 68 %).In order to explain this decrease of HC II level in dialyzed patients with CRF, we compared both AT III and HC II activities before and after a dialysis session in 24 patients (12 with a low and 12 with normal before dialysis HC II activity). AT III and HC II increased significantly (p < 0.01) in all patients after dialysis. When related to total plasma proteins in order to suppress the influence of hemoconcentration induced by dialysis, AT III decreased significantly (p < 0.01) in the 24 patients while HC II increased significantly (p < 0.01) only in patients with low before dialysis HC II levels (the increase in HC II activity was found significantly in the pooled 24 patients).

Elevation Of Antithrombin III By Sulfinpyrazone Therapy In Chronic Renal Failure

1981 ◽  
Author(s):  
M Bern ◽  
J Green
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Antithrombin Iii ◽  
Chronic Hemodialysis ◽  
Protective Effects ◽  
Platelet Factor ◽  
At Iii ◽  
Before And After ◽  
Artery Disease ◽  
And Function

Sulfinpyrazone can reduce the incidence of thrombosis of A-V shunts in chronic renal failure. The drug is also reported to prevent acute deaths from coronary artery disease. This study was to determine mechanisms for these protective effects.Patients on chronic hemodialysis served as the study models. Six patients on dialysis three times per week for 6 or more months received sulfinpyrazone 200 mgm t.i.d. p.o. for 14 days. Blood samples were obtained before dialysis was begun before and after the 14 days of drug therapy.Results are shown as mean ± standard error of mean.AT III levels rose significantly by functional and immune assays. Functional levels (by von Kaulla technique) rose 24.5 ± 3.1 sec. to 47.3 + 5.5 sec. (P>.005) Plasma protein AT III (by radial immunodiffusion) rose 31.2 ± 2.17 mg/dl to 37.9 ± 2.1 mgm/dl. (P>.01) Platelet factor 4 (by Abbot radioimmunology assay) fell from 46.4 + 13.6 ngm/ml to 9.5 ± 1.1 ngm/ml.(P>.005) The concentration of thrombin-anti-thrombin complex (by R. Rosenberg, Harvard Medical School, Boston) rose from 4.2 ± .09 to 8.4 ± 1.0 (P>.005)Thus it appears that sulfinpyrazone elevates antithrombin concentration and function while simultaneously suppressing platelet release. These two effects may or may not be mutually dependent. The clinical efficacy of sulfinpyrazone may relate in part to the elevation of antithrombin III, probably by inhibiting its consumption, while also inhibiting platelet function.

Distribution of antithrombin III in rabbits: role of host and protein

1987 ◽  
Vol 252 (3) ◽  
pp. R457-R461
Author(s):  
E. Regoeczi
Keyword(s):  
Plasma Proteins ◽  
Antithrombin Iii ◽  
The Body ◽  
Unknown Mechanism ◽  
A Value ◽  
Catabolic Rate ◽  
At Iii ◽  
Body Compartments ◽  
The Relationship

Unlike in the case of some other species, the plasma curve of iodine-labeled antithrombin III (I-AT-III) in rabbits requires fitting with a three-term exponential function for obtaining reliable estimates of the catabolic rate and distribution of I-AT-III among various body compartments (Carlson, Atencio, and Simon. J. Clin. Invest. 74: 191-199, 1984). To decide whether this phenomenon is referable to the host or the protein, the behavior of rabbit and human I-AT-III was comparatively analyzed in rabbits. Data obtained with rabbit I-AT-III confirmed the findings by Carlson and co-workers. Human I-AT-III assumed a distribution that closely paralleled that of homologous I-AT-III, thus suggesting that the pattern of distribution is determined by the host species rather than its AT-III. Rabbits metabolized human I-AT-III 1.61 times faster than homologous I-AT-III by an unknown mechanism not involving immune response; a facet that may prove useful for the identification of the sites of catabolism of AT-III. The exponent of the body weight was calculated for the relationship between species size and AT-III turnover. A value of 0.5 was obtained that is distinctly lower than the exponents found earlier for some other plasma proteins.

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