Introduction:
Hypercoagulability is a risk factor for early renal allograft loss (1,2). We report the successful renal transplantation with perioperative supplementation of fresh frozen plasma(FFP) in a patient with antithrombin (AT) deficiency.
Methods:
Case: A 42-year-old, 52-kg, nonsmoking male with anuria due to IgA nephropathy and unremarkable family history was scheduled to receive a live-donor kidney transplantation from wife. At hemodialysis(HD) initiation he developed right axillary, subclavian and internal jugular vein (IJV) thrombosis after insertion of a dialysis catheter in right IJV. He was started on apixaban 2.5 mg BD. His subclavian and axillary vein thrombus resolved. He remained on HD by a left IJV cuffed catheter. After twelve weeks of thrombotic event, apixaban was stopped for two days and detailed workup revealed evidence of AT deficiency (66% of normal) and normal other tests. (Table-1). A congenital AT deficiency was entertained as he did not have risk factors for acquired AT deficiency including nephrotic syndrome, liver disease, or estrogen etc. Apixaban stopped two days before and the patient hospitalized 1 day before the scheduled live-donor renal transplantation. As the AT concentrates or recombinant AT were not available, four units of FFP 250 ml each, were given twelve hours before surgery. Induction therapy included Basiliximab 20 mg on day 0 and 4, methylprednisolone, mycophenolate mofetil (MMF), and tacrolimus. In addition, 5000 units of heparin was given IV prior to clamping of the iliac vessels. Patient started making urine output on table. Postoperatively, 5,000 units of subcutaneous heparin was started every 8 hr. The graft functioned successfully and he achieved nadir creatinine of 0.92 mg/dL on day-3. Doppler evaluation of graft vessels showed normal flow. Heparin was converted to injection enoxaparin 40 mg subcutaneously from day-1 to 10 and followed by apixaban 2.5 mg BD. Post discharge patient is doing well.
Table -1
Results:
AT is a serine-protease inhibitor of thrombin, and factor Xa. AT functions as endogenous anticoagulant and its deficiency manifests as hypercoagulability and heparin resistance. Patients with congenital AT deficiency require life-long anticoagulation. When temporary anticoagulation cessation is needed in AT deficient patients, the ensuing thrombotic risk can be minimized with the administration of either plasma derived AT concentrates (pdAT) or the recombinant human AT (rhAT). If antithrombin III concentrates are not available, FFP at a dose of 20 mL/kg can raise the AT-III level by approximately 20% (3). Infusion of 1000ml FFP increased AT activity to 86%, which is considered safe. Pooled normal human plasma pdAT has a half-life of 3.8 days (4) therefore FFP were transfused twelve hours before planned surgery during hemodialysis. Perioperative FFP use in our patient has enabled us to avoid early postoperative anticoagulation thus balancing the risk of thrombosis versus hemorrhage. LMWH use in later peri operative period provided desired anticoagulation. (3).
Conclusions:
This shows that kidney transplantation can be performed safely in AT-deficient patients under FFP cover if recombinant AT or plasma derived AT concentrates are not available. It is also cost effective compared to recombinant AT therapy.
I have no potential conflict of interest to disclose.
I did not use generative AI and AI-assisted technologies in the writing process.