Hypotension During Sham Apheresis in a Patient Taking ACE Inhibitors

Hypotensive reaction during staphylococcal protein A column therapy in a patient with anomalous degradation of bradykinin and Des‐Arg9‐bradykinin after contact activation

“…To study formation and degradation of kinins, exposed her plasma to glass beads. We found a normal kinin formation rate but an abnormal degradation and accumulation of Des‐Arg 9 ‐BK. The kinin degradation enzymes ACE, aminopeptidase P (APP), and carboxypeptidase N (CPN) were measured while on an ACE inhibitor, showing absence of ACE activity, low APP, but normal CPN. CONCLUSION : This patient's vasodilation and hypotension during SPA therapy was associated with a pre‐ existing anomaly of BK metabolism.…”

“…The kinin degradation enzymes ACE, aminopeptidase P (APP), and carboxypeptidase N (CPN) were measured while on an ACE inhibitor, showing absence of ACE activity, low APP, but normal CPN. CONCLUSION : This patient's vasodilation and hypotension during SPA therapy was associated with a pre‐ existing anomaly of BK metabolism. Her ACE inhibitor shifted degradation toward Des‐Arg 9 ‐BK formation, and her low APP was associated with a prolonged t 50 and accumulation of the vasoactive Des‐Arg 9 ‐BK.…”

Bradykinin metabolism and hypotensive transfusion reactions

“…During LDL apheresis, LDL cholesterol is adsorbed to low‐molecular‐weight dextran sulfate covalently bound to cellulose on the columns. Some patients taking ACE inhibitors experienced hypotension, erythematous skin (particularly on the face and neck), bradycardia, nausea, and sometimes other symptoms such as dyspnea, sweats, headache, and abdominal pain 103–111 . These symptoms started shortly after the treated plasma was returned to the patient and subsided within minutes of discontinuing the transfusion.…”

“…They also showed that the use of thrombin and the kallikrein inhibitor nafamostat mesilate, instead of heparin, as anticoagulant prevents elevations of plasma BK levels during LDL apheresis and acute hypotensive reactions. It is interesting that Petrucco et al 111 demonstrated that, even with sham LDL apheresis, in which plasma is separated by the negatively charged, hollow polysulfone filter and reinfused without passing through the dextran sulfate‐cellulose LDL column, a patient taking ACE inhibitors can have acute hypotensive reactions.…”

“…Some patients taking ACE inhibitors experienced hypotension, erythematous skin (particularly on the face and neck), bradycardia, nausea, and sometimes other symptoms such as dyspnea, sweats, headache, and abdominal pain. [103][104][105][106][107][108][109][110][111] These symptoms started shortly after the treated plasma was returned to the patient and subsided within minutes of discontinuing the transfusion. The symptoms were reproduced by restarting the plasma transfusion.…”