Table 1. Proposed pathophysiological mechanisms of contrast-induced acute kidney injury [adapted from reference (25)].

Medullary vasoconstriction and hypoxia

Direct cytotoxicity to renal tubular cells

Release of vasoconstrictive mediators: Endothelin, adenosine, angiotensin II, vasopressin

Reduction of vasodilatatory mediators: Nitric oxide, prostocyclin

Increased oxidative stress

Impairment of tubulo-glomerular feedback

Increased blood and renal tubular viscosity

Impairment of mitochondrial function and mitochondrial membrane potential