Heparins and blood polymorphonuclear stimulation in haemodialysis: an expansion of the biocompatibility concept

Leitienne, Philippe; Fouque, Denis; Rigal, Dominique; Adeleine, P.; Trzeciak, Marie‐Christine; Laville, Maurice

doi:10.1093/ndt/15.10.1631

Cited by 19 publications

(15 citation statements)

References 27 publications

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“…In another study comparing heparin-free and conventional dialysis using a CU membrane, there was no fall in platelet count 30 min into conventional dialysis using heparin, and the results were not different from heparin-free dialysis. 58 Leitienne et al 59 compared the effects of dialysis using a CT membrane with four different heparin protocols, using either unfractionated heparin or low-molecular-weight heparin, studying each of the compounds at two different doses. Although the degree of leucopenia and leukocyte elastase were increased with unfractionated heparin versus low-molecular-weight heparin, the decreases in platelet counts with the four anticoagulation regimens were similar.…”

Section: Heparin Effect On Platelets and Heparin-induced Thrombocytopmentioning

confidence: 99%

Hemodialysis effect on platelet count and function and hemodialysis-associated thrombocytopenia

Daugirdas

Bernardo

2012

Kidney International

171

149

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Substantial activation of platelets can occur in the course of hemodialysis. Platelet surface markers show evidence of platelet degranulation. Some activation occurs due to exposure of blood to the roller pump segment and microbubbles may play a role. Platelet activation seems to be reduced with reused dialyzers or with those containing synthetic versus cellulosic membranes. Nevertheless, a substantial degree of platelet activation can be demonstrated with polysulfone and other synthetic membranes; the amount of activation may differ substantially among polysulfone membranes, depending on the manufacturer and the polyvinylpyrrolidone content. Platelet-platelet and platelet-leukocyte aggregates have been detected in the dialyzer blood outflow line and the consequences of these to the microcirculation are unknown. Typically, the platelet count decreases slightly during the first hour of dialysis, but mostly returns to initial values by the end of dialysis. A number of chronic hemodialysis patient cases have been reported in which a marked decrease in platelet count (50% or more) during dialysis was observed, resulting in mild degrees of predialysis thrombocytopenia. In only one case was the decrease in platelet count associated with bleeding. Dialyzer hypersensitivity symptoms are infrequently associated with a fall in platelet count. Most recent cases of dialysis-associated thrombocytopenia have been with polysulfone membranes, especially polysulfone membranes sterilized by electron beam. The exact cause of these reactions remains unknown.

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Section: Heparin Effect On Platelets and Heparin-induced Thrombocytopmentioning

confidence: 99%

Hemodialysis effect on platelet count and function and hemodialysis-associated thrombocytopenia

Daugirdas

Bernardo

2012

Kidney International

171

149

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“…Heparin binds to lipopolysaccharide-binding protein, and this binding facilitates the transfer of lipopolysaccharide to the CD14 receptor, thereby augmenting the endotoxin-induced activation of monocytes [9,18]. It should be noted that, for the prevention of clotting of the extracorporeal circuit, higher doses of heparins are often required, increasing the risk of proinflammatory effects [9,29]. …”

Section: Heparinmentioning

confidence: 99%

Clinical review: Anticoagulation for continuous renal replacement therapy - heparin or citrate?

2010

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Heparin is the most commonly prescribed anticoagulant for continuous renal replacement therapy. There is, however, increasing evidence questioning its safety, particularly in the critically ill. Heparin mainly confers its anticoagulant effect by binding to antithrombin. Heparin binds to numerous other proteins and cells as well, however, compromising its efficacy and safety. Owing to antithrombin consumption and degradation, and to the binding of heparin to acute phase proteins, and to apoptotic and necrotic cells, critical illness confers heparin resistance. The nonspecific binding of heparin further leads to an unpredictable interference with inflammation pathways, microcirculation and phagocytotic clearance of dead cells, with possible deleterious consequences for patients with sepsis and systemic inflammation. Regional anticoagulation with citrate does not increase the patient's risk of bleeding. The benefits of citrate further include a longer or similar circuit life, and possibly better patient and kidney survival. This needs to be confirmed in larger randomized controlled multicenter trials. The use of citrate might be associated with less inflammation and has useful bio-energetic implications. Citrate can, however, with inadequate use cause metabolic derangements. Full advantages of citrate can only be realized if its risks are well controlled. These observations suggest a greater role for citrate.

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“…Leitienne et al [19] showed that the proinflammatory mediator release during hemodialysis depends on heparin dose. In addition, Gritters et al [20] found that myeloperoxidase and platelet factor 4 were released into the systemic circulation directly after the infusion of heparin before connection of the extracorporeal circuit.…”

Section: Patient and Kidney Survivalmentioning

confidence: 99%

Citrate Anticoagulation for Continuous Renal Replacement Therapy in the Critically Ill

Straaten

2010

Blood Purif

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Background: Heparins are used for circuit anticoagulation during continuous renal replacement therapy (CRRT). Because heparins cause systemic anticoagulation, they increase the risk of bleeding. Citrate provides regional anticoagulation. Since citrate is a buffer as well, its use has metabolic consequences. The preferential use of citrate therefore remains controversial. Methods: A synthesis was performed of published studies comparing citrate to heparin for anticoagulation in CRRT with specific regard to feasibility, efficacy and safety. Search of the literature was made to explain the reported superiority of citrate. Results: Citrate provides good metabolic control if and when a well-designed protocol is strictly followed. Randomized studies report similar or longer circuit survival with citrate compared to heparin and less bleeding. The largest randomized trial up to now found that citrate was better tolerated than heparin and improved patient and kidney survival, especially in patients after surgery, with sepsis, a high degree of organ failure or younger age. Both citrate and heparin interfere with inflammation. Conclusion: During critical illness, regional anticoagulation with citrate for CRRT seems superior to heparin anticoagulation concerning tolerance and safety, mainly due to less bleeding. Whether circuit survival is better depends on the modality. In addition, citrate seems to improve patient and kidney survival. This finding needs to be confirmed. Citrate seems to confer a specific benefit in severe organ failure and sepsis. To what extent citrate protects or heparin does harm in the setting of multiple organ failure needs to be unraveled.

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Heparins and blood polymorphonuclear stimulation in haemodialysis: an expansion of the biocompatibility concept

Cited by 19 publications

References 27 publications

Hemodialysis effect on platelet count and function and hemodialysis-associated thrombocytopenia

Hemodialysis effect on platelet count and function and hemodialysis-associated thrombocytopenia

Clinical review: Anticoagulation for continuous renal replacement therapy - heparin or citrate?

Citrate Anticoagulation for Continuous Renal Replacement Therapy in the Critically Ill

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