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2005; Akimoto et al. 2011]. In the Oklahoma TTP registry, malignant hypertension (n?=?6) was determined to be the underlying cause of TMA referred for plasma exchange in about 2% of cases [George, 2010]. Despite these figures, our review showed only 18 GNAT2 reported cases with detailed information. Thus, malignant hypertension-induced TMA is likely to be unrecognized and under-reported. However, differentiating TTP and malignant hypertension-induced TMA is meaningful from both therapeutic and prognostic standpoints. Many experts believe that plasma exchange should be considered in TTP after the exclusion of alternate causes such severe malignant hypertension, implying that the presence of a severe malignant hypertension excludes TTP [Schwartz et al. 2013]. However, TTP literature does not provide explicit information about the extent of hypertension noted in TTP patients. Importantly, one-third of reported cases of malignant hypertension-induced TMA have undergone plasma exchange, thus highlighting the clinical dilemma in reliably differentiating the two conditions and foregoing plasma exchange based on initial clinical suspicion. Our review presents several important similarities and differences between malignant hypertension-induced TMA and TTP. Both TTP and malignant hypertension-induced TMA mostly present with neurological and gastrointestinal symptoms. In malignant hypertension-induced TMA, however, patients do not have fever. Prior history of hypertension and higher mean arterial pressure at presentation are possible clues to a diagnosis of malignant hypertension. The greater degree of renal impairment at diagnosis, relatively modest thrombocytopenia and lack of severe ADAMTS-13 deficiency (activity excretion at admission among malignant hypertension patients with versus without microangiopathic hemolyic anemia [van den Born et al. 2005]. Akimoto and colleagues showed a higher serum creatinine, lower hemoglobin and lower platelet count among malignant hypertension patients with versus without TMA; however, the difference was not statistically significant likely because of small number of patients [Akimoto et al. 2011]. These prior publications, based on institutional experiences, focus on the comparison of patients with malignant hypertension with versus without microangiopathy, rather than with TTP. The use of plasma exchange and ADAMTS-13 level are not extensively discussed. Table 2. Comparison of different series of malignant hypertension-induced thrombotic microangiopathy and patients in the Oklahoma Thrombotic Thrombocytopenic Purpura Registry with ADAMTS-13??10%.