Haemostasis in kidney failure

Abstract

Introduction to the pathophysiology of haemostasis in kidney failure The haemostatic system is a finely balanced biological mechanism that maintains an equilibrium between the procoagulant and anticoagulant pathways. This complex system is dynamic, whereby the procoagulant pathway is set in motion in cases of vascular injury to ensure haemostasis, while the anticoagulant pathway prevents excessive blood clotting (thrombosis). Kidney failure (KF), that is the final and permanent stage of chronic kidney disease (CKD), knocks this delicate balance out of kilter, making KF patients susceptible to both thrombotic and bleeding episodes. The pathophysiology of this paradox is intricate and multifactorial. Increased thrombotic risks are attributed to chronic inflammation and endothelial cell damage, whereas bleeding tendencies are associated with primary haemostatic interferences and anaemia of chronic disease3. Risks of thromboembolic complications tend to be exacerbated in KF due to accompanying comorbidities such as cardiovascular disease (CVD) and diabetes mellitus (DM). CKD is a persistent and progressive condition affecting more than 850 million individuals worldwide4. Kidney Disease Improving Global Outcomes (KDIGO) guidelines define KF as aglomerularfiltration rate (GFR)that is less than 15 ml/min/1.73 m2. At this stage patients are typically required to undergo long-term dialysis treatment or kidney transplantation.