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 temporal relationship of acute kidney injury developing within 2 days of contrast-enhanced CT administration in a 70-year-old patient. 1

Clinical Reasoning

Temporal Relationship and Mechanism

• Contrast-induced AKI typically manifests within 24-48 hours (up to 2-5 days) after contrast administration, which precisely matches this patient's presentation 1
• The pathophysiology involves renal medullary ischemia from contrast-induced vasoconstriction combined with direct tubular cytotoxicity, resulting in acute tubular necrosis 2, 3
• The mechanism includes reduced renal perfusion, decreased tubular flow, and direct tubular toxicity leading to decreased glomerular filtration rate 4

Why ATN Rather Than Other Options

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

• The patient's vital signs are stable (BP 130/70 mmHg, HR 76/min) without evidence of volume depletion 1
• Pre-renal states typically respond to volume expansion, whereas contrast-induced ATN represents intrinsic renal damage 4

Acute interstitial nephritis (Option C) is less likely because:

• AIN typically develops over days to weeks after drug exposure, not within 48 hours 1
• The clinical presentation lacks typical features of allergic interstitial nephritis 1

Acute glomerular nephritis (Option D) is unlikely because:

• The temporal relationship strongly suggests contrast toxicity rather than glomerular disease 1
• Glomerulonephritis would not typically present this acutely after contrast exposure 1

Risk Factors Present

This 70-year-old patient has advanced age, which is a recognized risk factor for contrast-induced nephropathy 1:

• Pre-existing renal impairment is the most critical risk factor for developing contrast-induced AKI 1, 4
• Elderly patients have higher baseline risk even without documented prior renal dysfunction 1
• The elevated creatinine (378 μmol/L) and urea (30.4 mmol/L) indicate significant renal injury has occurred 1

Pathophysiology of Contrast-Induced ATN

The mechanism involves multiple concurrent processes 2, 4:

• Altered renal hemodynamics with initial vasodilation followed by prolonged vasoconstriction 2
• Regional hypoxia particularly affecting the renal medulla 2, 3
• Direct cytotoxic effects on tubular epithelial cells 2, 4
• Increased fluid viscosity in distal tubular segments leading to tubular obstruction 2

Clinical Significance

• Contrast-induced nephropathy is the third most common cause of hospital-acquired acute renal failure 3
• It is associated with increased morbidity and in-hospital mortality 3
• In cancer patients with pre-existing kidney disease, 50% of contrast-induced nephropathy cases result in irreversible renal damage 1

Common Pitfall

The major pitfall is attributing all post-contrast AKI to the contrast agent when other causes may be present 1. However, in this case, the classic temporal relationship (2 days post-contrast), absence of other obvious causes, and typical presentation make contrast-induced ATN the most likely diagnosis 1.