Anticoagulant action of low, physiologic, and high albumin levels in whole blood

Abstract

Albumin is the most abundant plasma protein. Critical illness is often associated with altered, predominately decreased, serum albumin levels. This hypoalbuminaemia is usually corrected by administration of exogenous albumin. This study aimed to track the concentration-dependent influence of albumin on blood coagulation in vitro. Whole blood (WB) samples from 25 volunteers were prepared to contain low (19.3 ± 7.7 g/L), physiological (45.2 ± 7.8 g/L), and high (67.5 ± 18.1 g/L) levels of albumin. Haemostatic profiling was performed using a platelet function analyzer (PFA) 200, impedance aggregometry, a Cone and Platelet analyzer (CPA), calibrated automated thrombogram, and thrombelastometry (TEM). Platelet aggregation-associated ATP release was assessed via HPLC analysis. In the low albumin group, when compared to the physiological albumin group, we found: i) shortened PFA 200-derived closure times indicating increased primary haemostasis; ii) increased impedance aggregometry-derived amplitudes, slopes, ATP release, as well as CPA-derived average size indicating improved platelet aggregation; iii) increased TEM-derived maximum clot firmness and alpha angles indicating enhanced clot formation. TEM measurements indicated impaired clot formation in the high albumin group compared with the physiological albumin group. Thus, albumin exerted significant anticoagulant action. Therefore, low albumin levels, often present in cancer or critically ill patients, might contribute to the frequently occurring venous thromboembolism.

Hypoalbuminemia for the prediction of venous thromboembolism and treatment of direct oral anticoagulants in metastatic gastric cancer patients

“…Several previous studies suggest that albumin affects blood coagulation system. Pear M et al revealed significant anticoagulant properties of albumin in vitro [36]. According to this study, albumin inhibits the deposition of platelets in the primary hemostasis and impairs fibrinogen activity by interacting with fibrinogen [36].…”

“…Pear M et al revealed significant anticoagulant properties of albumin in vitro [36]. According to this study, albumin inhibits the deposition of platelets in the primary hemostasis and impairs fibrinogen activity by interacting with fibrinogen [36]. Maclouf J et al showed that albumin inactivates thromboxane A2, which is capable of inducing platelet aggregation, directly through binding [37].…”

Hyperthermic intraperitoneal chemotherapy enhances blood coagulation perioperatively evaluated by thromboelastography: a pilot study

“…The role of albumin in terms of blood coagulation is controversial. In vitro, low albumin level increased ROTEM maximum clot firmness [32]. On the other hand, extreme dilution with albumin is associated with coagulopathy in TEG [33].…”

Platelet adhesion on commercially pure titanium plates in vitro I: effects of plasma components and involvement of the von Willebrand factor and fibronectin

“…However, Sivaraman and Lautour [24] proposed that in its adsorption state, serum albumin changes the structure of a large number of charged amino acids (i.e., 24 arginine, 59 lysine, 35 aspartic acid, and 62 glutamic acid residues) recognized by Arg-Gly-Asp (RGD)-specific receptors in platelets similar to an RGD motif. In addition, studies have reported that serum albumin shows significant anticoagulant action in a concentration-dependent manner [26]. According to this theory, serum albumin that remained in platelet pellets produced by centrifugation might be able to support initial platelet adhesion in collaboration with other genuine adhesion molecules.…”