, pp. 203 - 238, 2020/01/01.
The retained metabolic products in kidney insufficiency are toxic to two main cells connected with blood coagulation, namely, the endothelial cells and the blood platelets. These interact with each other, with leukocytes and with a complex metabolic network involving inflammation, complement activation, coagulation, fibrinolysis, and others. Owing to the unstable nature of kidney insufficiency, the associated coagulation disorders vary from a procoagulant state where endothelial cell injury predominates, to a bleeding disorder where platelet dysfunction supervenes. Amid all that, patients with kidney insufficiency may need anticoagulation either for the commonly associated heart disease, venous thrombosis, antiphospholipid syndrome, etc., for the treatment of certain intrinsic renal disease, or for extracorporeal therapy. This requires a careful benefit/risk balance that can be quantitated by validated scores. As the decision to anticoagulate is made, several practical issues emerge, including the choice of pharmacokinetically compatible agents, their dose in relation to the degree of impairment of kidney function, and potential drug-drug interactions. The decision is confounded by the plethora of currently available anticoagulants, often with superior efficacy, less bleeding tendency, and limited need for monitoring and frequent dose tailoring compared to the traditional heparin and warfarin.
]