Assessment of haemostasis and impact of fibrinogen supplementation on clot properties using global haemostasis assays in patients on chronic dialysis

Abstract

Patients with end-stage renal disease (ESRD) are at increased risk of haemostasis disorders which result from changes in plasma and platelet (PLT) components [1]. Haemodialysis (HD) is the most common method of treatment used in patients with ESRD [2]. The contact between blood and the artificial surfaces of dialysis machines increases PLT reactivity and the production of coagulation factors. Consequently, this may lead to the occurrence of coagulopathy. It may also affect the natural process of blood clot dissolution (fibrinolysis) [3]. Concomitantly, damage in the vascular endothelium and changes in the activity of proteins participating in the coagulation cascade during the course of the ESRD may pose a risk of haemorrhage [1]. Furthermore, HD may only replace about 10% of proper

Association between Functional Parameters of Coagulation and Conventional Coagulation Tests in the Setting of Fluid Resuscitation with Balanced Crystalloid or Gelatine: A Secondary Analysis of an In Vivo Prospective Randomized Crossover Study

“…As mentioned above, a comparison between ROTEM and conventional tests of fibrinogen and platelet concentration also reported sufficient agreement between the results in an in vivo setting, which is relevant when considering fibrinogen as the key coagulation factor [ 29 ]. Based on the observations of the correlation between viscoelastic and conventional coagulation tests, there is a trend for trusting the viscoelastic methods in the POC setting during goal-directed, personalized fluid resuscitation [ 30 ], concerning the coagulopathies developing in patients on chronic dialyses [ 31 ] or recently in the identification and risk stratification of thromboembolic events in patients suffering from COVID-19 [ 32 , 33 ]. Importantly, not all studies have taken into account blood dilution in their investigations.…”

“…Firstly, the cohort was small, and no a priori sample size calculation was done. We based the study group size on the available published literature with similar study methodology [ 30 , 31 ]. Moreover, to increase the reliability of our results, we performed additional a posteriori power calculations regarding our study’s sample size for the study group.…”

Navigating through the haemostatic paradox in kidney failure: A practical overview

“…Haemostatic alterations in relation to renal failure were first reported by Giovanni Battista Morgagni in his “Opera Omnia” in 1764, 8 and despite major scientific advancements, haemostatic management still proves to be elusive 9 . This is because the pathophysiology of renal coagulopathy is both multifactorial and paradoxical, meaning that kidney failure patients are susceptible to both thrombotic 10,11 and bleeding 12,13 diathesis (Table 1). Pathogenesis of thrombotic events is consequential to endothelial cell damage and inflammation, 14 whereas bleeding episodes tend to occur due to anaemia and primary haemostatic interferences, 15,16 courtesy of uraemic toxins.…”