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Angiotensin-converting enzyme (ACE) inhibitors have previously been associated with flushing and hypotension in patients undergoing TPE. Patients undergoing TPE have an activation of the prekallikrein and bradykinin system on contact with the extracorporeal membranes. ACE inhibitors potentiate this reaction by inhibiting bradykinin catabolism. Angiotensin receptor blockers (ARBs) have also been postulated to cause elevated bradykinin levels although data pertaining to the use of ARBs in TPE is limited. We hope to highlight this rare inter
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