A new Low Molecular Weight Heparinoid Org 10172 as Anticoagulant in Hemodialysis

Bonsdorff, Mikaela von; Stiekema, J. C. J.; Harjanne, Aira; Alapiessa, U.

doi:10.1177/039139889001300209

Cited by 14 publications

(3 citation statements)

References 15 publications

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“…In cases of suspected HIT, danaparoid may therefore have an increased thera-/ peutic window in patients with acute renal failure as ; compared with r-hirudin. A single bolus injection of danaparoid is a useful and safe alternative anticoagulant dur-/ ing hemodialysis (10)(11)(12)(13), while only limited data about application in venovenous hemofiltration in critically ill ' patients are available (14).…”

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confidence: 99%

Use of a Low-Molecular-Weight Heparinoid (Danaparoid Sodium) for Continuous Renal Replacement Therapy in Intensive Care Patients

Lindhoff-Last

Betz

Bauersachs

2001

Clin Appl Thromb Hemost

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The purpose of this study was to evaluate the efficacy and safety of danaparoid in the treatment of critically ill patients with acute renal failure and suspected heparin-induced thrombocytopenia (HIT) needing renal replacement therapy (RRT). We conducted a retrospective analysis of 13 consecutive intensive care patients with acute renal failure and suspected HIT who were treated with danaparoid for at least 3 days during RRT. In eight patients, continuous venovenous hemofiltration was performed. The mean infusion rate of danaparoid was 140 +/- 86 U/hour. Filter exchange was necessary every 37.5 hours. In five patients, continuous venovenous hemodialysis was used. A bolus injection of 750 U danaparoid was followed by a mean infusion rate of 138 +/- 122 U/hour. Filters were exchanged every 24 hours. In 7 of 13 patients, even a low mean infusion rate of 88 +/- 35 U/hour was efficient. Mean anti-Xa (aXa) levels were approximately 0.4 +/- 0.2 aXa U/mL. Persistent thrombocytopenia despite discontinuation of heparin treatment was observed in 9 of 13 patients, owing to disseminated intravascular coagulation (DIC). HIT was confirmed by an increase in platelet count and positive heparin-induced antibodies in 2 of 13 patients. No thromboembolic complications occurred, but major bleeding was observed in 6 of 13 patients, which could be explained by consumption of coagulation factors and platelets due to DIC in 5 of 6 patients. Nine of 13 patients died of multiorgan failure or sepsis, or both. In none of these patients was the fatal outcome related to danaparoid treatment. In critically ill patients with renal impairment and suspected HIT, a bolus injection of 750 U danaparoid followed by a mean infusion rate of 50 to 150 U/hour appears to be a safe and efficient treatment option when alternative anticoagulation is necessary.

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confidence: 99%

Use of a Low-Molecular-Weight Heparinoid (Danaparoid Sodium) for Continuous Renal Replacement Therapy in Intensive Care Patients

Lindhoff-Last

Betz

Bauersachs

2001

Clin Appl Thromb Hemost

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“…Die Antikoagulation für Hämodialysepatienten mit HIT-II inkludiert -die Gabe von rekombinantem Hirudin (z.B. Lepirudin) in einer Bolusdosierung von 0,08-0,15 mg/kg mit Beginn der Dialysebehandlung, -die Gabe von PEG (Polyethylenglykol)-Hirudin als Bolusinjektion in einer Dosierung von 0,04-0,08 mg/ kg, -die Gabe von Danaparoid-Natrium (Orgaran), -die regionale Antikoagulation mit Zitrat [220][221][222][223][224][225][226][227][228][229][230].…”

Section: Heparin-induzierte Thrombozytopenieunclassified

Platelet dysfunction in Uremia

Hörl

2006

Wien Klin Wochenschr

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Bleeding diathesis and thrombotic tendencies are characteristic findings in patients with end-stage renal disease. The pathogenesis of uremic bleeding tendency is related to multiple dysfunctions of the platelets. The platelet numbers may be reduced slightly, while platelet turnover is increased. The reduced adhesion of platelets to the vascular subendothelial wall is due to reduction of GPIb and altered conformational changes of GPIIb/IIIa receptors. Alterations of platelet adhesion and aggregation are caused by uremic toxins, increased platelet production of NO, PGI(2), calcium and cAMP as well as renal anemia. Correction of uremic bleeding is caused by treatment of renal anemia with recombinant human erythropoietin or darbepoetin alpha, adequate dialysis, desmopressin, cryoprecipitate, tranexamic acid, or conjugated estrogens. Thrombotic complications in uremia are caused by increased platelet aggregation and hypercoagulability. Erythrocyte-platelet-aggregates, leukocyte-platelet-aggregates and platelet microparticles are found in higher percentage in uremic patients as compared to healthy individuals. The increased expression of platelet phosphatidylserine initiates phagocytosis and coagulation. Therapy with antiplatelet drugs does not reduce vascular access thrombosis but increases bleeding complications in endstage renal disease patients. Heparin-induced thrombocytopenia (HIT type II) may develop in 0-12 % of hemodialysis patients. HIT antibody positive uremic patients mostly develop only mild thrombocytopenia and only very few thrombotic complications. Substitution of heparin by hirudin, danaparoid or regional citrate anticoagulation should be decided based on each single case.

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“…Danaparoid has been used successfully to manage hemodialysis (HD) in patients with HIT. 42,43,[78][79][80][81][82] Before beginning hemodialysis, the anti-factor Xa activity should be monitored. Once the optimal dose is identified, it can often be used with less frequent periodic measurement of anti-factor Xa activity.…”

Section: Hemodialysismentioning

confidence: 99%

Treatment of Heparin-Induced Thrombocytopenia

Greinacher¹

1999

Thromb Haemost

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IntroductionUnfractionated heparin (UFH) and low molecular weight heparin (LMWH) are the most widely used anticoagulants when parenteral anticoagulation with a short half-life is required. Both can be administered subcutaneously and intravenously, and both have been shown to be effective in a variety of clinical settings.1 UFH has several limitations. One is its poor bioavailability after subcutaneous injection and the marked variability in its anticoagulant response in patients with an acute thromboembolic complication.2,3 Another major issue associated with UFH is the induction of heparin-induced thrombocytopenia (HIT). Both limitations are closely linked,4 as the underlying cause is the high density of negative charges on the heparin molecule and its molecular weight. Both are responsible for the binding of heparin to plasma proteins other than antithrombin (AT), such as platelet factor 4 (PF4) and to several cell types. This leads to heparin-platelet interaction, the formation of HIT antigen (i.e., PF4/heparin complexes), and inhibition of the anticoagulant effect of heparin (aPTT-nonresponder).

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A new Low Molecular Weight Heparinoid Org 10172 as Anticoagulant in Hemodialysis

Cited by 14 publications

References 15 publications

Use of a Low-Molecular-Weight Heparinoid (Danaparoid Sodium) for Continuous Renal Replacement Therapy in Intensive Care Patients

Use of a Low-Molecular-Weight Heparinoid (Danaparoid Sodium) for Continuous Renal Replacement Therapy in Intensive Care Patients

Platelet dysfunction in Uremia

Treatment of Heparin-Induced Thrombocytopenia

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