A hypothetical case study: a patient whose birthdate was 9-20-1945 had ESRD and non-valvular atrial fibrillation. He had been on renal dialysis since 2011 and had been taking Coumadin since 2005, maintaining an INR of 2.7, even after dialysis was initiated. In the summer of 2014 he experienced a soft-tissue bleed, prompting his nephrologist to discontinue Coumadin. In the fall of 2014 he developed deep venous thrombosis that was treated with unfractionated heparin. Shortly after the DVT he experienced a stroke and he expired late in 2014. The stroke was neither defined as hemorrhagic or ischemic.
George has read that 15% of renal dialysis patients also have non-valvular atrial fibrillation. It seems that nephrologists and cardiologists walk a tightrope when treating dialysis patients with Coumadin. Is there any means by which the coagulation laboratory could have contributed to this patient’s care, for instance, by offering PIVKA assays–proteins in vitamin K antagonist therapy–or chromogenic factor X assays to more accurately measure Coumadin effects? Could the laboratory have predicted the risk of a DVT? Is there an effective way of monitoring heparin therapy in dialysis patients? Please offer your opinions in the comments section below.
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