What is the most likely cause of impaired renal function in a patient with elevated urea and creatinine levels, who underwent a contrast-enhanced computed tomography (CT) brain scan 2 days ago?

Acute Tubular Necrosis from Contrast-Induced Nephropathy

The most likely mechanism for this patient's renal impairment is acute tubular necrosis (ATN) secondary to contrast-induced acute kidney injury (CI-AKI), given the temporal relationship of symptom onset 2 days after contrast-enhanced CT and the significantly elevated creatinine (378 µmol/L). 1

Pathophysiologic Mechanism

CI-AKI is an intrinsic renal process, not a pre-renal condition. The mechanism involves:

• Direct tubular toxicity from reactive oxygen species generated by the contrast medium 1, 2
• Renal medullary ischemia resulting from contrast-induced vasoconstriction and altered renal hemodynamics 1, 2
• Direct cellular damage to tubular epithelial cells from the contrast agent itself 1
• Decreased glomerular filtration and renal hypoperfusion contributing to tubular injury 2

Clinical Presentation Consistent with CI-AKI

The timing is pathognomonic for contrast-induced injury:

• CI-AKI typically presents with serum creatinine rise within 48 hours (up to 5 days) following contrast administration 3, 1
• This patient's presentation at 2 days post-contrast fits the classic timeframe 3
• Most episodes of CI-AKI are nonoliguric, which is consistent with this patient's presentation 3

Why Not the Other Options

Pre-renal azotemia (Option A) is incorrect because:

• The patient has normal vital signs (BP 130/70, HR 76/min) without evidence of volume depletion 3
• Pre-renal states are functional and reversible with volume repletion, whereas CI-AKI represents structural tubular damage 2
• The temporal relationship to contrast exposure points to intrinsic renal injury 1

Acute interstitial nephritis (Option C) is unlikely because:

• AIN typically presents with fever, rash, eosinophilia, and pyuria—none mentioned here 3
• The timeframe is more consistent with CI-AKI than allergic interstitial nephritis 1

Acute glomerular nephritis (Option D) is unlikely because:

• No evidence of hematuria, proteinuria, or systemic features of glomerulonephritis 3
• The mechanism of contrast injury targets tubules, not glomeruli 1, 2

Risk Factors Present

Pre-existing renal impairment is the principal risk factor for CI-AKI, and while baseline creatinine is not provided, the patient's age and vascular disease history (TIA evaluation) suggest underlying chronic kidney disease 3

Clinical Pitfalls to Avoid

• Do not assume all post-contrast renal dysfunction is pre-renal—the mechanism is intrinsic tubular injury requiring different management 1
• Do not confuse CI-AKI with atheroembolic disease, which can also occur post-catheterization but presents differently with livedo reticularis, eosinophilia, and progressive rather than acute onset 4
• Recognize that hemodynamically stable patients can still develop CI-AKI—normal blood pressure does not exclude the diagnosis 1

Answer: B. Acute tubular necrosis