Haemostasis in liver disease

Haemostasis in kidney failure is marked by a paradoxical coexistence of bleeding and thrombotic risks. The bleeding tendency mainly results from qualitative platelet dysfunction due to uremic toxins, endothelial abnormalities and the aggravating effect of anemia. Clinically, this manifests as mucocutaneous bleeding, gastrointestinal haemorrhage and excessive bleeding during invasive procedures. At the same time, patients are predisposed to thrombotic events through mechanisms including chronic inflammation, dialysis-related factors, vascular access devices and elevated procoagulant proteins such as fibrinogen, factor VIII and von Willebrand factor.

Diagnosis remains challenging, as conventional coagulation tests are often normal and do not reflect the haemostatic imbalance. Platelet function assays and global haemostatic tests may provide additional insights but lack standardization and predictive accuracy in this setting.

Management strategies must be individualized. Correction of anemia improves platelet function, while dialysis helps reduce circulating toxins but introduces anticoagulation-related risks. Desmopressin is useful in acute bleeding episodes, though its effect is transient. Anticoagulation may be necessary for thrombosis prevention, but dosing and drug selection require careful adaptation to altered pharmacokinetics and heightened bleeding risk.

Overall, haemostasis in kidney failure represents a fragile equilibrium. A better understanding of the underlying mechanisms, along with careful diagnostic and therapeutic strategies, is essential to optimize outcomes in this high-risk population.
During this webinar, clinicians, clinical pathologists, PhDs and clinical laboratory staff will have the opportunity to explore these mechanisms, review current diagnostic challenges and discuss strategies for individualized patient management.