Anticoagulation in chronic kidney disease patients-the practical aspects

Abstract

There is an increasing awareness about the risks of arterial and venous thromboembolism (TE) in hospital patients and general public which has led to consideration of thrombosis prevention measures in earnest. Early recognition of the symptoms of TE disease has led to timely administration of antiplatelet and anticoagulant drugs, translating to better outcome in many of these patients. In this respect, patients with chronic kidney disease (CKD) represent a special group. They indeed represent a high-risk group for thrombosis both in the cardiovascular territory and also in the venous circulation. At the same time, abnormalities in the platelet membranes put them at risk of bleeding which is significantly more than other patients with chronic diseases. Anticoagulation may be ideal to prevent the former, but the co-existing bleeding risk and also that the commonly used drugs for inhibiting coagulation are eliminated by renal pathways pose additional problems. In this review, we try to explain the complex thrombotic-haemorrhagic state of chronic kidney disease patients, and practical considerations for the management of anticoagulation in them with a focus on heparins.

Keywords: anticoagulation; heparin; thrombosis; warfarin.

Fig. 1.

Heparin binds to AT which potentiates its anti-Xa and AT effects. The AT-thrombin effect does require the long-chain, while the anti-XA effect requires only the pentasaccharide sequence.

Fig. 2.

Coagulation starts by tissue factor binding to factor VII. This activates some factor X which will cause a small, initial thrombin burst. This thrombin will activate factors VIII and IX, which will activate further factor X leading to huge thrombin burst. The sites of action of the newer oral anticoagulants and direct thrombin inhibitors are shown.