In this episode of Hospital Medicine Unplugged, we unpack contrast-induced nephropathy (CIN)—spot the risks, flood the kidneys (not the lungs), cut the contrast, and prevent a hospital-acquired AKI before it starts.

We open with the do-firsts: identify high-risk inpatients—those with CKD (especially eGFR <30), diabetes, heart failure, advanced age, or prior contrast within 72 hours. Draw a baseline creatinine and estimate GFR pre-procedure; no shortcuts here. Intra-arterial studies (PCI, angiography) carry more risk than IV contrast CTs.

Call CIN when you see a rise in creatinine ≥0.5 mg/dL or ≥25% from baseline within 48–72 hours post-contrast, after excluding other causes (hypotension, nephrotoxins, atheroemboli). The KDIGO AKI definition is now preferred—≥0.3 mg/dL increase within 48h or 1.5× baseline within 7 days, or urine output <0.5 mL/kg/h for ≥6h.

Pathophysiology plays:
Contrast agents inflict direct tubular toxicity and indirect medullary ischemia. They cause vasoconstriction via endothelin, blunt nitric oxide, increase oxidative stress, and heighten viscosity—all of which tank renal perfusion. Tubular epithelial injury → cell swelling, necrosis, obstruction, and reduced GFR. Medullary hypoxia seals the deal.

Risk-stratify before you inject (any = high risk):
• CKD (eGFR <60; highest if <30)
• Diabetes (esp. with CKD)
• Age >75, heart failure, volume depletion, hypotension
• High contrast volume (>350 mL or >4 mL/kg), intra-arterial route, repeat studies <72h
• Nephrotoxins (NSAIDs, aminoglycosides, IV amphotericin, diuretics)
• Acute coronary syndromes or mechanical circulatory support during PCI

Clinical course: Creatinine rises in 24–72h, peaks day 3–5, and normalizes in 1–3 weeks if reversible. Usually non-oliguric, but oligo/anuria = severe. Dialysis need is rare (<2%), but mortality spikes if required.

Prevention—build the hydration backbone:
• Isotonic saline (0.9%) at 1 mL/kg/h for 6–12h pre- and post-contrast (shorter 3+6h for urgent PCI).
• Sodium bicarbonate (e.g., 250 mL 1.4% over 1h pre-, then 1 mL/kg/h for 6h post-) is an alternative, but not superior (PRESERVE, JAMA 2020).
• Oral hydration ≠ enough for high-risk inpatients.
• Hold nephrotoxins around the procedure.
• Use the lowest feasible contrast volume and choose iso- or low-osmolar media.
• Avoid repeat contrast studies within 72h.

Adjuncts (evidence weak but low-risk):
• N-acetylcysteine 600–1200 mg BID, start before and continue after—may help, can’t hurt.
• High-dose statins (e.g., atorvastatin 80 mg) may lower CIN risk in PCI.
• No role for dopamine, fenoldopam, theophylline, or prophylactic dialysis.

If CIN develops:
• Supportive only—maintain euvolemia, stop nephrotoxins, monitor urine and labs.
• Dialysis only for standard triggers (refractory hyperkalemia, acidosis, overload, uremia).
• No therapy reverses established CIN—time, fluids, and vigilance are your tools.
• Recheck creatinine daily for 3–5 days, then space if stable.

Key lab trends:
Creatinine ↑ by ≥0.5 mg/dL or ≥25% within 48–72h → peaks day 3–5 → resolves by week 2.
Early shifts (≥5% in 12h) predict persistent damage. NGAL and cystatin C rise earlier but aren’t yet routine.

Hospital protocol that sticks:

1. Screen: all contrast orders → auto-prompt for eGFR.

2. Hydrate: isotonic saline 1 mL/kg/h (adjust in CHF).

3. Hold: nephrotoxins 24h pre/post.

4. Limit: contrast dose and repetition.

5. Check: creatinine at 48–72h post-exposure.

6. Document: CIN episode in EHR for future contrast precautions.

System moves:
Bundle prevention into radiology workflow—automatic hydration orders, contrast dose calculators, EHR alerts for eGFR <45, and follow-up creatinine flags at 48h.

Bottom line—CIN is preventable, predictable, and high-stakes. Hydrate early, minimize contrast, skip the nephrotoxins, and track the creatinine curve. Prevention beats dialysis every time.