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 48-hour timeframe following contrast-enhanced CT and the patient's advanced age as a risk factor. 1

Clinical Reasoning

Temporal Relationship Points to Contrast Toxicity

• Contrast-induced AKI typically manifests within 24-48 hours (up to 2-5 days) after contrast administration, which precisely matches this patient's presentation two days post-procedure. 1
• The timing is pathognomonic for contrast-induced nephropathy rather than other causes of acute kidney injury 1, 2
• This narrow time window after iodinated contrast exposure is the defining characteristic that distinguishes contrast-induced ATN from other renal pathologies 3

Why Not Pre-renal Azotemia (Option A)

• Pre-renal azotemia is excluded because the patient has stable vital signs (BP 130/70 mmHg, HR 76/min) without evidence of volume depletion or hemodynamic instability 1
• There are no clinical signs of hypovolemia, hypotension, or decreased renal perfusion that would suggest a pre-renal etiology 1
• The stable hemodynamics argue strongly against inadequate renal perfusion as the primary mechanism 1

Why Not Acute Interstitial Nephritis (Option C)

• Acute interstitial nephritis typically develops over days to weeks after drug exposure, not within 48 hours 1
• The rapid onset within 2 days is inconsistent with the typical time course of allergic interstitial nephritis 1
• This diagnosis would require a longer latency period and often presents with fever, rash, and eosinophilia, which are not mentioned 1

Why Not Acute Glomerular Nephritis (Option D)

• The temporal relationship strongly suggests contrast toxicity rather than glomerular disease 1
• Glomerulonephritis typically presents with hematuria, proteinuria, and edema over a more protracted course 1
• There is no clinical context suggesting immune-mediated glomerular injury 1

Pathophysiology of Contrast-Induced ATN

The mechanism involves multiple concurrent pathways:

• Direct tubular cytotoxicity from contrast media causes cellular injury and necrosis 2, 4
• Contrast-induced reduction of renal perfusion leads to regional hypoxia in the medulla 2, 4
• Increased fluid viscosity and reduced tubular flow contribute to tubular obstruction 2, 4
• Reactive oxygen species and vasoactive mediators (adenosine, endothelin) exacerbate tubular damage 2

Risk Factors Present in This Patient

• Advanced age (70 years) is a recognized risk factor for contrast-induced nephropathy 1, 5
• Elderly patients have higher baseline risk even without documented prior renal dysfunction 1
• The patient may have had subclinical renal impairment that was not previously detected, which is the most critical risk factor for developing contrast-induced AKI 5, 4

Clinical Significance and Prognosis

• In 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
• Even when acute renal failure does not require dialysis, patients experience diminished long-term survival 6

Common Pitfall to Avoid

Do not assume normal baseline renal function in elderly patients without recent creatinine measurements. The elevated creatinine of 378 μmol/L suggests either pre-existing chronic kidney disease that was unrecognized or severe acute injury on top of baseline impairment. 5 The dramatic elevation indicates this patient was likely at high risk before the procedure but was not adequately screened. 5