Do not use Continuous Venovenous Hemodialysis in the Setting of Angiotensin-Converting Enzyme 2 and Vice Versa



Do not use Continuous Venovenous Hemodialysis in the Setting of Angiotensin-Converting Enzyme 2 and Vice Versa


Anthony D. Slonim MD, DRPH



Kinins are a group of peptides that have strong vasodilating properties. They are formed from large precursor molecules named kininogens by the action of proteolytic enzymes called kallikreins, which are formed in the liver. Kallikreins exist peripherally as prekallikreins, which become activated through a number of different mechanisms including exposure to Hageman factor (factor XII) from the coagulation system and artificial surfaces including dialysis membranes. Rapid deactivation occurs for most kinins after formation to prevent the body from having an overwhelming response to these powerful substances.

Bradykinin, however, is an example of a kinin that has a longer half-life. It is formed from its precursor kallidin, which is a product of low-molecular-weight kininogen in the tissues. Bradykinin is a physiologically active product that has several functions. It can act on the vascular endothelium to reduce smooth muscle tone and cause vasodilatation. It is also active during acute inflammation as a signal to the generation of arachidonic acid–derived products such as prostaglandins and leukotrienes. In addition, bradykinin becomes activated during activation of the clotting cascade and tissue repair mechanisms. Finally, there is a potential role for bradykinin in hypertension since it is involved in the conversion of prorenin to renin and levels appear to be reduced in patients with hypertension.

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Jul 1, 2016 | Posted by in ANESTHESIA | Comments Off on Do not use Continuous Venovenous Hemodialysis in the Setting of Angiotensin-Converting Enzyme 2 and Vice Versa

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