Effect of Renal Function on the Pharmacodynamics of Argatroban

Arpino, Paul A.; Hallisey, Robert K.

doi:10.1345/aph.1d163

Cited by 57 publications

(52 citation statements)

References 10 publications

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“…34 Several reports, each describing a small number of patients, have reported the use of argatroban in patients requiring renal replacement therapy. [16][17][18][19]21,26,31,[35][36][37][38][39][40][41][42] Dialytic clearance of argatroban with high-flux membranes has been suggested to be clinically insignificant, with systemic clearance increased by about 20%. 36,37 Many authors have reported using doses less than 0.5 µg/kg per minute to achieve aPTT of 40-80 s, but some of the patients were critically ill, with acute changes in liver function or recent cardiovascular surgery, or they may have had volume overload, with subsequent hepatic congestion.…”

Section: Discussionmentioning

confidence: 99%

“…[8][9][10][11][12][13][14] Furthermore, for patients with acute cardiac disease and those in the intensive care unit (ICU), a dose of 2 µg/kg per minute may lead to a supratherapeutic aPTT if liver function is normal, which could potentially increase the risk of hemorrhagic complications. 12,13,[15][16][17][18] Others have found the need for dose modifications in patients with renal impairment, 14,[19][20][21][22] which contradicts the manufacturer's information.…”

Section: Introductionmentioning

confidence: 99%

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Clinical Experience with Argatroban for Heparin-Induced Thrombocytopenia in a Large Teaching Hospital

Bates¹,

Griffin

Angel³

2009

CJHP

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Background: Argatroban is a direct thrombin inhibitor approved for the prophylaxis or treatment of thrombosis in patients with heparininduced thrombocytopenia (HIT). The product monograph does not guide clinicians beyond specifying the initial dose of 2 µg/kg per minute (or 0.5 µg/kg per minute for patients with hepatic impairment). Some authors have suggested that in the intensive care unit (ICU) and for patients with acute cardiac disease and those with renal or hepatic dysfunction, this dose may result in a supratherapeutic activated partial thromboplastin time (aPTT).

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Clinical Experience with Argatroban for Heparin-Induced Thrombocytopenia in a Large Teaching Hospital

Bates¹,

Griffin

Angel³

2009

CJHP

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“…In patients with renal failure it has been suggest lower dosing requirements with dose reduction of approximately 0.1 to 0.6 μg/kg/min for each 30 ml/min decrease in the creatinine clearance. (Hursting, 2008;Arpino, 2004) …”

Section: Argatrobanmentioning

confidence: 99%

Venous Thromboembolism in Neonates, Children and Patients with Chronic Renal Disease – Special Considerations

Lázaro¹,

Arriola²,

Romero³

et al. 2012

Pathophysiology and Clinical Aspects of Venous Thromboembolism in Neonates, Renal Disease and Cancer Patients

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“…It must be noted that the dosing in Table I is not FDA approved and was developed by amassing information from the literature as well as incorporating in-hospital data and pharmacists' experiences with dosing argatroban. The doses are adjusted for hepatic and/or renal dysfunction based partly on recommendations from the manufacturer as well as data from published sources [12]. After the initiation of the argatroban infusion, the patient's aPTT was above the target goal.…”

Section: Commentarymentioning

confidence: 99%

Argatroban and catheter‐directed thrombolysis with alteplase for limb‐ and graft‐threatening thromboses in a patient with a history of HIT

Maldonado

2009

American J Hematol

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A 73-year-old, 6 0 0@, 130 kg, white male who is selfemployed as a farmer presented to the hospital with a chief complaint of severe nausea, vomiting, and diarrhea accompanied by dizziness and diaphoresis occurring since that morning. His family and social history were noncontributory. On examination, the patient appeared comfortable and in no acute distress. The blood pressure was 92/56 mmHg, the pulse 68 beats per minute, the temperature 97.68F, the respiratory rate 18 breaths per minute, and the oxygen saturation 95% on room air. Lung sounds were diminished bilaterally in the bases. The remainder of a 10-point review of systems was negative except for an elevated serum creatinine (1.6, 1.2 mg/dL baseline), BUN (30 mg/dL), and white blood cell count (14.4 K/lL).The patient's initial presentation was consistent with a bacterial or viral gastroenteritis along with acute renal failure secondary to volume depletion. Other factors that predisposed him to gastrointestinal symptoms included longterm immunosuppression with mycophenolate mofetil as well as uremia.The patient has an extensive medical history that includes relevant disease states. The patient is 5 years post living donor kidney transplant secondary to chronic renal failure from ischemic nephropathy. His course immediately following transplant was complicated by deep venous thromboses in the right femoral and popliteal veins and pulmonary embolism secondary to hypercoagulability disorders including documented elevated anticardiolipin IgM antibody and protein S deficiency in the setting of a normal protein C level. Heparin and warfarin therapy had been initiated at the time of diagnosis. He developed thrombocytopenia and a heparin-induced thrombocytopenia (HIT) antibody test was reported in the record as weakly positive. He was subsequently treated with fondaparinux and warfarin but developed a diverticular bleed within 1 month. Anticoagulation was discontinued and an inferior vena cava filter was placed. The patient then opted against chronic anticoagulation. His current medications at the time of admission include alendronate, allopurinol, aspirin, calcium carbonate, carvedilol, ferrous sulfate, fish oil, furosemide, glipizide, multivitamins, mycophenolate mofetil, pantoprazole, prednisone, tacrolimus, and tamsulosin. His listed allergies include an unknown reaction to atenolol, itching with cephalexin, and heparin-induced thrombocytopenia.Upon admission, blood, stool, and urine cultures were obtained and subsequently were negative. FK506 and MMF levels were within normal limits making it unlikely that drug toxicity was causing his symptoms. An unenhanced abdominal CT demonstrated acute diverticulitis and the patient was started on ciprofloxacin and metronidazole for treatment.On the 2nd day of admission, the patient's serum creatinine continued to rise and he became oliguric. He also developed bilateral lower extremity edema, pain, cyanosis, and mottling. Due to his worsening renal function, the patient developed metabolic acidosis and because of this, ...

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Effect of Renal Function on the Pharmacodynamics of Argatroban

Abstract: Estimated Cl(cr) significantly predicted the dose of argatroban needed to reach a therapeutic aPTT.

Cited by 57 publications

References 10 publications

Clinical Experience with Argatroban for Heparin-Induced Thrombocytopenia in a Large Teaching Hospital

Clinical Experience with Argatroban for Heparin-Induced Thrombocytopenia in a Large Teaching Hospital

Venous Thromboembolism in Neonates, Children and Patients with Chronic Renal Disease – Special Considerations

Argatroban and catheter‐directed thrombolysis with alteplase for limb‐ and graft‐threatening thromboses in a patient with a history of HIT

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