{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T20:06:24Z","timestamp":1777406784814,"version":"3.51.4"},"reference-count":37,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2009,1,20]],"date-time":"2009-01-20T00:00:00Z","timestamp":1232409600000},"content-version":"vor","delay-in-days":19,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Clinical Apheresis"],"published-print":{"date-parts":[[2009,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background:<\/jats:title><jats:p>Thrombotic microangiopathy (TMA) encompasses a number of disorders with hemolytic anemia and thrombocytopenia, including thrombotic thrombocytopenic purpura (TTP). A deficiency in ADAMTS13 enzyme levels, along with an inhibitory antibody, is found in most patients with idiopathic TTP. Patients with human immunodeficiency virus (HIV) infection can have a TTP\u2010like illness; however, it appears to have a different etiology.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods:<\/jats:title><jats:p>A retrospective review of patients who had an ADAMTS13 activity level performed from 2005 through 2007 was completed. Patients with a diagnosis of HIV infection with TMA were investigated.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results:<\/jats:title><jats:p>Two patients were identified. Case 1: a 47\u2010year\u2010old man with HIV infection and a CD4 count &lt;10\/\u03bcL presented with altered mental status, pneumonia, acute renal failure, thrombocytopenia, and anemia. The ADAMTS13 level was 71%. He was treated with plasma infusion. Two days after admission, he expired because of respiratory distress syndrome and metabolic lactic acidosis. Case 2: a 39\u2010year\u2010old man with HIV infection and a CD4 count of 9\/\u03bcL presented with chest pain, acute renal failure, thrombocytopenia, and anemia. The ADAMTS13 level was 65%. He received multiple units of fresh frozen plasma without significant improvement in his platelet count. Six days after admission, the patient began highly active antiretroviral therapy, which resulted in a rapid increase in his platelet count.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions:<\/jats:title><jats:p>HIV\u2010associated TMA is postulated to have a different pathophysiology than idiopathic TTP. This study supports that assumption because both patients exhibited many of the classic findings of TTP but did not have a deficiency of ADAMTS13. J. Clin. 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