Which of the following is true about contrast-induced nephropathy (CIN) in patients undergoing procedures with radiocontrast agents, particularly those with pre-existing renal impairment?

Contrast-Induced Nephropathy: True Statement Analysis

Direct Answer

Radiocontrast agents mediate vasoconstriction and markedly affect renal parenchymal oxygenation, especially in the outer medulla is the TRUE statement. 1

Pathophysiologic Mechanism

The correct answer reflects the established pathophysiology of contrast-induced nephropathy (CIN):

• Contrast media causes direct renal medullary ischemia through vasoconstriction, particularly affecting the outer medulla where oxygen tension is already low, combined with direct tubular toxicity and cellular damage from reactive oxygen species 1
• The pathogenesis is multifactorial, involving decreased glomerular filtration, renal hypoperfusion, and direct cellular toxicity from the contrast agent itself 1
• Multiple mechanisms work synergistically: interference with renal perfusion, altered glomerular permeability, direct tubular injury, and intraluminal obstruction 2

Why the Other Statements Are FALSE

Statement 1: "They typically present with oliguria"

• This is incorrect - most episodes of CIN are nonoliguric 1
• Oliguria is associated in only approximately 30% of cases, not the typical presentation 2
• The majority of contrast-enhanced procedures occur in outpatient settings where urine output monitoring is impractical, further emphasizing that oliguria is not the defining feature 1

Statement 2: "Peak serum creatinine concentration seen in 7 days"

• This is incorrect - the peak serum creatinine occurs within 3-5 days after contrast exposure, not 7 days 2
• CIN is defined by a rise in serum creatinine ≥0.5 mg/dL or ≥25% from baseline within 48 hours after contrast exposure 1
• The temporal relationship shows onset of increased creatinine within 24 hours, with peak at 3-5 days 2

Statement 4: "The fractional excretion of sodium is >1%"

• This is incorrect - CIN is an intrinsic renal process involving direct tubular toxicity and renal medullary ischemia 1
• As an intrinsic renal injury (not prerenal), CIN would typically present with FENa >1%, but this statement is misleading because it's not a defining characteristic used clinically for diagnosis
• The diagnosis relies on serum creatinine changes, not FENa measurements 1, 2

Clinical Implications

• Pre-existing renal insufficiency is the single most influential risk factor, with patients having serum creatinine >2 mg/dL at nearly 10-fold increased risk 1
• When diabetes coexists with renal impairment, the incidence of CIN approaches very high levels 2
• Prevention focuses on intravenous hydration with isotonic saline (1.0-1.5 mL/kg/hour) for 3-12 hours before and 6-24 hours after contrast exposure, minimizing contrast volume, and using low-osmolar or iso-osmolar contrast media 3, 4