What is the role of vasoconstriction in the etiology of contrast-induced nephropathy (CIN)?

Updated: Dec 18, 2018
  • Author: Anita Basu, MD, FACP; Chief Editor: Vecihi Batuman, MD, FASN  more...
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Answer

CM-mediated vasoconstriction is the result of a direct action of CM on vascular smooth muscle and from metabolites such as adenosine and endothelin. Additionally, the osmotic property of CM, especially in the tubular lumen, decreases water reabsorption, leading to a buildup of interstitial pressure. This, along with the increased salt and water load to the distal tubules, reduces GFR and causes local compression of the vasa recta. All of this contributes to worsening medullary hypoxemia and renal vasoconstriction in patients who are already volume depleted.

Finally, CM also increases resistance to blood flow by increasing blood viscosity and by decreasing red cell deformability. The resulting intravascular sludging generates local ischemia and causes activation of reactive oxygen species that cause tubular damage at a cellular level.


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