Table 5.

Proposed pathophysiological mechanisms of contrast-induced acute kidney injury

Medullary vasoconstriction and hypoxia[27-29]

Direct cytotoxicity to renal tubular cells[30-33]

Release of vasoconstrictive mediators: Endothelin, adenosine, angiotensin II, vasopressin[28]

Reduction of vasodilatatory mediators: Nitric oxide, prostocyclin[28,32,34]

Increased oxidative stress[32,35,36]

Impairment of tubulo-glomerular feedback[32]

Increased blood and renal tubular viscosity[41]

Impairment of mitochondrial function and mitochondrial membrane potential[42]