Abstract

Acute hypotensive transfusion reactions (AHTRs) are characterized by early and abrupt onset of hypotension as the predominant clinical manifestation. The drop in blood pressure typically resolves quickly once the transfusion is stopped. Disturbances in the production and metabolism of bradykinin cause the pathophysiology of these reactions. Bradykinin is produced after Factor XII becomes activated due to contact with negatively charged surfaces such as tubing systems, dialysis membranes, and blood filters used for leukoreduction. Bradykinin, a vasoactive peptide that binds to receptors on the endothelium and causes hypotension, is primarily metabolized by the angiotensin converting enzyme (ACE). An increase in the recognition of AHTRs has been due to the growing use of ACE inhibitors, the use of negatively charged leukoreduction filters and both genetic and induced alterations in bradykinin kinetics. This review describes the epidemiology of AHTRs, current understandings about the pathophysiology, and prevention measures.

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