Approach this by attacking the root cause rather than adding a drug. Contrast nephropathy stems largely from the osmotic and direct toxic burden of the iodinated agent on the renal tubules and medulla, so the single most dependable safeguard is to give a contrast medium that imposes less of that burden.
Low-osmolar (and iso-osmolar) contrast media carry a much lower osmotic load than the older high-osmolar agents. In a patient who already has reduced renal reserve, choosing such an agent directly lessens medullary hypoxia and tubular injury, which is why it is the preferred option when the goal is to prevent contrast-induced kidney damage.
The drug-based choices are weaker. N-acetylcysteine as an antioxidant has given conflicting trial results and is not a guaranteed protector. Fenoldopam, a selective dopamine-1 agonist, has failed to show consistent renal protection. Mannitol, an osmotic diuretic, provides no protective benefit and can even aggravate the situation. So none of them outranks simply selecting a safer contrast agent.
The preferred measure is therefore the safer contrast medium.
\[\boxed{\text{Low osmolar contrast media}}\]