What is the most likely cause of impaired renal function in a patient with elevated urea and creatinine levels after a contrast-enhanced computed tomography (CT) scan?

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 nephropathy, given the characteristic presentation of elevated creatinine developing within 48 hours of contrast-enhanced CT administration. 1

Temporal Relationship Confirms Contrast-Induced ATN

• Contrast-induced AKI typically manifests within 24-48 hours (up to 2-5 days) after contrast administration, which precisely matches this patient's 2-day timeline. 1
• The peak serum creatinine occurs within 3-5 days of the contrast study, consistent with this presentation. 2
• This temporal pattern is the defining clinical feature that distinguishes contrast-induced nephropathy from other causes of acute kidney injury. 2

Why Other Mechanisms Are Less Likely

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

• The patient has stable vital signs with blood pressure 130/70 mmHg and heart rate 76/min, showing no evidence of volume depletion or hemodynamic instability. 1
• There are no clinical features suggesting inadequate renal perfusion such as hypotension, tachycardia, or dehydration. 1

Acute interstitial nephritis (Option C) is unlikely because:

• This condition typically develops over days to weeks after drug exposure, not within 48 hours. 1
• The rapid onset within 2 days points away from an allergic or inflammatory mechanism. 1

Acute glomerular nephritis (Option D) is improbable because:

• The temporal relationship strongly suggests contrast toxicity rather than glomerular disease. 1
• There is no mention of proteinuria, hematuria, or other features of glomerulonephritis. 1

Pathophysiology of Contrast-Induced ATN

The mechanism involves both renal ischemia and direct tubular toxicity:

• Contrast media cause altered renal hemodynamics leading to regional hypoxia in the renal medulla. 3, 4
• Direct cytotoxic effects on renal tubular cells occur from the contrast agent itself. 3, 5
• Increased fluid viscosity in the tubular system can lead to obstruction and further tubular damage. 3
• The combination of ischemic injury and direct cellular toxicity results in acute tubular necrosis. 4

Clinical Significance and Prognosis

• In cancer patients with pre-existing kidney disease, 50% of contrast-induced nephropathy cases result in irreversible renal damage. 1
• Contrast-induced nephropathy is associated with increased morbidity and in-hospital mortality. 1
• Oliguria is associated in approximately 30% of cases of contrast-induced nephropathy. 2

Critical Risk Factors Present

Advanced age is a recognized risk factor for contrast-induced nephropathy, making elderly patients particularly vulnerable even without documented prior renal dysfunction. 1

Answer: B. Acute tubular necrosis is the correct mechanism, as this represents the pathophysiologic consequence of contrast-induced nephropathy occurring within the characteristic 24-48 hour timeframe after contrast administration. 1, 3, 4