Thrombotic thrombocytopenic purpura (TTP) is an acute, life-threatening illness 
with disseminated platelet-rich thromboses of small vessels that variably 
presents with the classic clinical "pentad" of microangiopathic hemolytic 
anemia, thrombocytopenia, fever, altered mental status, and acute kidney injury. 
Most cases are caused by an acquired autoantibody to ADAMTS13, a 
metalloproteinase that cleaves large von Willebrand Factor (vWF) multimers. The 
mainstay of treatment is daily therapeutic plasma exchange (TPE), sometimes with 
adjunctive pharmacologic immunosuppression. TPE is generally continued until the 
platelet count is greater than 150 × 103 /µL and the lactate dehydrogenase is 
near normal for 2-3 consecutive days. Unfortunately, there is no clear guidance 
for when thrombocytopenia is refractory for a prolonged period of time. The 
following case describes such a scenario in which consecutive ADAMTS13 activity 
and inhibitor levels were used to guide the decision to stop treatment with TPE 
in a patient who failed to recover their platelet count.