Contrast nephropathy
Contrast nephropathy
Contrast Nephropathy — 20 MCQs
Select an option for each question. After your selection the correct option will be highlighted in light green-yellow and your incorrect selection (if any) will appear light red. Explanations are revealed after each attempt.
1. Which of the following best defines contrast-induced nephropathy (traditional definition)?
Traditional criteria: increase in creatinine ≥0.5 mg/dL or ≥25% within 48–72 hours of contrast, after excluding other causes. Newer definitions sometimes use ≥0.3 mg/dL.
2. The predominant pathophysiologic mechanisms in contrast nephropathy include:
Contrast causes renal vasoconstriction → medullary ischemia and direct tubular cell toxicity; oxidative stress also contributes.
3. Which patient is at highest risk for contrast nephropathy?
Major risk factors include pre-existing CKD (reduced eGFR), diabetes, older age, heart failure, dehydration, and nephrotoxic drugs.
4. Which preventive measure has the strongest evidence for reducing risk of contrast nephropathy?
Isotonic IV hydration before and after contrast is the mainstay prevention strategy. Evidence for NAC is mixed; routine post-procedure dialysis is not recommended.
5. Which contrast characteristic is associated with lower nephrotoxicity?
Iso- and low-osmolality agents are less nephrotoxic than older high-osmolality agents; minimizing contrast volume also reduces risk.
6. Which of the following hydration protocols is commonly recommended for prevention in patients at risk (not heart failure)?
Isotonic saline 1 mL/kg/h (usually 6–12 h pre and 4–12 h post) is commonly recommended; adjust rate in heart failure. Diuretics are not protective unless used with monitored hydration strategies.
7. When should repeat contrast administration generally be avoided?
Close repeat exposures (within 48–72 h) increase risk, especially in high-risk patients; plan imaging to avoid back-to-back contrast when possible.
8. Which drug should typically be withheld around the time of contrast exposure if possible?
NSAIDs are nephrotoxic and should be withheld around contrast exposure. Decisions on ACE inhibitors or metformin are individualized (metformin withheld if AKI risk), but NSAIDs are a clear risk factor.
9. What is the typical time course of serum creatinine after contrast-induced kidney injury?
Creatinine usually rises within 24–48 h, peaks around day 3–5, and often returns toward baseline by 7–10 days in uncomplicated cases.
10. Which statement about N‑acetylcysteine (NAC) for prevention is correct?
Trials show mixed results; NAC may be used as adjunct in some protocols but should not replace IV hydration. Routine universal use is not supported by high-quality evidence.
11. Which is NOT an established risk factor for contrast nephropathy?
Young healthy age alone is not a risk factor; established risks include CKD, diabetes, hypotension, heart failure, dehydration, and nephrotoxins.
12. For a patient on metformin undergoing contrast CT, recommended action is:
Guidelines suggest holding metformin around contrast if there is risk of AKI; check renal function and restart after 48 h if stable.
13. Which biomarker rises earlier than serum creatinine and has been studied for earlier detection of AKI?
NGAL and other novel biomarkers rise earlier than creatinine and have been studied for early AKI detection, but are not yet universally used in routine practice.
14. Which of the following procedural changes can reduce CIN risk?
Minimizing contrast volume and using lower-osmolality agents reduce risk. The other options raise risk or are unhelpful.
15. Which patients might benefit from individualized hydration strategies (slower or monitored) rather than standard fixed-rate hydration?
Heart failure patients may need tailored hydration (lower rates, hemodynamic monitoring) to avoid volume overload while still protecting kidneys.
16. Is immediate prophylactic hemodialysis after contrast recommended to prevent CIN?
Studies show routine immediate dialysis does not reliably prevent CIN and is not recommended unless patient already requires dialysis for other reasons.
17. Which clinical sign would most strongly suggest an alternative cause of AKI rather than CIN?
Sepsis, hypotension, or other insults can cause or contribute to AKI; always exclude other causes before labeling it contrast-induced.
18. Which monitoring is reasonable after contrast administration in high-risk patients?
High-risk patients should have renal function checked within 24–48 h; peak often at 3–5 days, so follow-up testing is reasonable based on clinical context.
19. Which statement about outcomes is true?
While many recover, CIN is linked to worse outcomes in patients with comorbidities. Permanent dialysis is uncommon but possible in severe cases.
20. Which intervention is most appropriate when a patient develops significant AKI after contrast?
Management is supportive: stop nephrotoxins, optimize volume status, monitor electrolytes and urine output, and consult nephrology for severe cases or dialysis indications.
Contrast Nephropathy — also called Contrast-Induced Nephropathy (CIN) or Contrast-Associated Acute Kidney Injury (CA-AKI) — is a form of acute kidney injury that occurs after administration of intravascular iodinated contrast media, typically used in imaging procedures such as CT scans, coronary angiography, or interventional radiology.
Definition
Traditionally defined as:
- An increase in serum creatinine by ≥0.5 mg/dL or ≥25% from baseline within 48–72 hours after contrast administration,
- In the absence of an alternative cause.
Pathophysiology
Involves two main mechanisms:
- Renal vasoconstriction → reduced renal blood flow and medullary ischemia.
- Direct tubular toxicity from contrast media.
Additional factors: oxidative stress, increased tubular workload, and reactive oxygen species generation.
Risk Factors
Patient-related:
- Pre-existing CKD (especially eGFR <60 mL/min/1.73 m²)
- Diabetes mellitus (especially with nephropathy)
- Age >75 years
- Heart failure
- Dehydration or hypovolemia
- Hypotension
- Concurrent nephrotoxic drugs (NSAIDs, aminoglycosides, amphotericin B, cyclosporine)
Procedure-related:
- Large contrast volume
- High-osmolality contrast agents
- Intra-arterial administration
- Multiple contrast exposures within 48–72 hrs
Clinical Course
- Typically non-oliguric AKI
- Creatinine rises within 24–48 hrs, peaks at 3–5 days, returns to baseline in 7–10 days in most cases.
- Usually reversible, but may worsen CKD or rarely cause dialysis dependence.
Diagnosis
- Based on temporal relationship between contrast exposure and creatinine rise.
- Exclude other causes (sepsis, hypovolemia, drug-induced nephropathy).
- No specific imaging or biopsy needed in most cases.
Prevention
Mainstay is prophylaxis:
- Hydration
- Isotonic saline (0.9% NaCl) 1 mL/kg/h for 6–12 h before and 4–12 h after procedure
(adjust for heart failure) - Sodium bicarbonate infusion is an alternative (controversial benefit)
- Isotonic saline (0.9% NaCl) 1 mL/kg/h for 6–12 h before and 4–12 h after procedure
- Use lowest possible contrast dose
- Use iso- or low-osmolality contrast media
- Avoid repeat contrast within 48–72 hrs
- Withhold nephrotoxic drugs (NSAIDs, aminoglycosides, certain antivirals)
- N-acetylcysteine — once widely used, but large trials show minimal or no benefit
- High-flux hemodialysis immediately after — not routinely recommended unless already dialysis-dependent.
Management
- Mostly supportive care
- Continue adequate hydration
- Stop nephrotoxins
- Dialysis if severe AKI with refractory volume overload, hyperkalemia, or uremia.
Prognosis
- Generally reversible in low-risk patients.
- Higher mortality in hospitalized patients, largely due to comorbid illness rather than CIN itself.
Key Points Table
| Feature | Description |
|---|---|
| Definition | AKI within 48–72h of contrast without other cause |
| Mechanism | Renal vasoconstriction + direct tubular toxicity |
| Risk factors | CKD, diabetes, age >75, dehydration, large contrast dose |
| Prevention | Hydration, low-dose low-osmolality contrast, avoid nephrotoxins |
| Management | Supportive; dialysis if indicated |
| Prognosis | Usually reversible; worse in high-risk groups |
