Apixaban in dialysis patients can be considered for those with heparin induced thrombocytopenia that need systemic anticoagulation and cannot tolerate heparin. Consider the following case study.
A 73-year-old man with End-stage kidney disease secondary to hypertension is seen during dialysis rounds in the outpatient clinic. The patient just began hemodialysis. While reviewing the labs, the nephrologist notes that the platelet count is 55,000. During rounds, the nurse reveals the patient had clotted a dialyzer circuit earlier this week and has concerns the current one may need to be replaced this treatment.
The patient had a graft placed in the past, but that thrombosed, and he is currently dialyzing through a tunneled hemocatheter.
Given the concern for heparin-induced thrombocytopenia, the heparin is stopped and antibodies against platelet factor-4-heparin complex are sent and return positive.
The patient is diagnosed with heparin induced thrombocytopenia, HIT. Apixaban (Eliquis) is prescribed.
HIT and Anticoagulation Management – Apixaban in Dialysis Patients
Patient Overview
The patient has a diagnosis of Heparin-Induced Thrombocytopenia (HIT), a history of thrombosis, and is in end-stage kidney disease (ESKD). Here, Apixaban (Eliquis) should be continued as part of the treatment plan.
Mechanism of Apixaban in dialysis patients
Apixaban is an oral anticoagulant that works by directly and selectively inhibiting Factor Xa, an essential enzyme in the blood coagulation cascade. This mechanism helps prevent thrombus formation.
Understanding HIT
HIT is a rare disorder that can occur after exposure to heparin.
There are two types of HIT:
Type 1 HIT: * Platelet count nadir is typically >100,000/µL, occurring 24–48 hours after heparin exposure. * It is not associated with bleeding or thrombosis; heparin therapy may continue.
Type 2 HIT: * Results from antibody formation targeting PF4 complexed to heparin, leading to platelet activation and thrombosis. * Defined by a decline in platelet count with absolute thrombocytopenia or a ≥ 50% decrease occurring approximately 5 days after heparin exposure. * Platelet count nadirs are typically between 50,000–80,000/µL. * Has a mortality rate of up to 30% and occurs in 2–3% of patients exposed to unfractionated heparin, UFH and <1% of those exposed to low-molecular weight heparin, LMWH. * All heparin therapy must be discontinued, including heparin-coated devices.
Management of HIT
Because of the increased risk of thrombosis after discontinuation of heparin, systemic anticoagulation with an alternative to heparin is necessary.
Key points include:
* Up to 50% of patients may develop thrombosis within 30 days after diagnosis. * Systemic anticoagulation is usually continued for at least 1 month in the absence of a thrombotic event and for ≥ 3 months if an event has occurred. * Critically ill patients or those with limb or life-threatening thromboembolism should be treated with parenteral agents like argatroban or bivalirudin. * Stable patients may use warfarin or direct oral anticoagulants (DOACs), but warfarin is contraindicated until platelet counts recover. Apixaban in dialysis patients is preferred.
Dialysis Considerations
Thrombosis of the dialysis circuit can occur even without a thrombophilic condition like HIT. Patients with end-stage renal disease (ESRD) often receive anticoagulation during dialysis to prevent clotting.
Key points include:
* Heparin is acceptable for dialysis circuit anticoagulation in the absence of HIT type 2. * A weight-based bolus dose is typically given at the start of treatment, followed by a continuous infusion, which is stopped 30–60 minutes before the end of treatment. * Enoxaparin, a type of LMWH, is not recommended for daily dialysis because of the risk of dose accumulation.
Alternative Anticoagulation Strategies
For patients with HIT type 2, systemic anticoagulation is required for 1–3 months. Apixaban in dialysis patients can provide the systemic anticoagulation. Options that only address circuit thrombosis, such as saline flushes and regional citrate anticoagulation, are inadequate until HIT therapy is completed.
Considerations to protect the circuit include:
* Isotonic saline boluses of 100–200 mL can be used to flush blood from the dialyzer and dialysis circuit. * Citrate anticoagulation can be achieved through infusion or dialysate containing citrate, which interferes with calcium-dependent coagulation processes. * This method may enhance dialysis efficiency and reduce circuit thrombosis compared to heparin-free dialysis.
Use of Argatroban
Argatroban is a direct thrombin inhibitor indicated for managing HIT type 2. Important points include:
* Dosed by continuous infusion, making it more suitable for hospitalized patients. * Outpatient use in a dialysis unit is complicated by the need for close monitoring and increased costs. * Continuous anticoagulation for 1–3 months is necessary, so argatroban use during dialysis alone does not provide the 24-7 coverage needed to protect the patient from further thrombosis risk.
