Table 2.
Agent | Administration | putative mechanism of action | evidence |
---|---|---|---|
Renal vasodilators (e.g. dopamine) | Oral or intravenous | Increased renal blood flow | Numerous studies failed to show benefit; some suggestions of harm94 |
Sodium bicarbonate | Intravenous | Increased pH of tubular urine | Unclear; might cause harm through pro-oxidant properties96,100 |
N-acetylcysteine | Oral or intravenous (treatment duration is controversial) | Antioxidant effects, reduction of reactive oxygen species | Mixed evidence, but seems to be beneficial101 |
Adenosine-receptor antagonists (theophylline and antagonists of adenosine receptor A1) | Oral or intravenous | Antagonism of adenosine-mediated vasoconstriction | Theophylline: some evidence of benefit112,113 Selective adenosine receptor A1 antagonists: preliminary animal116 and human113 data suggest that these agents increase GFR |
Statins (simvastatin and atorvastatin) | Oral | Pleiotropic, antioxidant, and anti-inflammatory effects | Conflicting results from trials125,126 |
Abbreviations: CIAKI, contrast-induced acute kidney injury; GFR, glomerular filtration rate.