Acute Tubular Necrosis (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 elevated creatinine (378 μmol/L) occurring 2 days after contrast-enhanced CT imaging. 1, 2
Clinical Reasoning
The diagnosis of contrast-induced acute kidney injury (CI-AKI) is established by:
- Temporal relationship: Renal dysfunction occurring within 48-72 hours after contrast administration 3, 2, 4
- Magnitude of injury: Serum creatinine rise of ≥44 μmol/L (0.5 mg/dL) or ≥25% from baseline 2, 5
- Exclusion of alternatives: No clinical evidence of pre-renal causes (normal vital signs, no hypotension), interstitial nephritis (no fever, rash, eosinophilia mentioned), or glomerulonephritis (no hematuria, proteinuria, or systemic features) 3
Why Not the Other Options?
Pre-renal Azotemia (Option A) - Incorrect
- Blood pressure 130/70 mmHg and heart rate 76/min indicate hemodynamic stability 3
- No evidence of volume depletion, hypotension, or decreased renal perfusion 3
- Pre-renal injury would typically present with more dramatic BUN:creatinine ratio elevation, though the elevated urea (30.4 mmol/L) suggests some component of volume contraction may coexist 6
Acute Interstitial Nephritis (Option C) - Incorrect
- No mention of fever, rash, or eosinophilia that characterize allergic interstitial nephritis 3
- Timing is more consistent with ATN than AIN, which typically occurs 7-10 days after drug exposure 7
Acute Glomerular Nephritis (Option D) - Incorrect
- No evidence of hematuria, proteinuria, edema, or systemic inflammatory features 3
- Clinical presentation lacks the nephritic syndrome characteristics 3
Pathophysiology of Contrast-Induced ATN
The mechanism involves multiple pathways 2, 4:
- Direct tubular toxicity via reactive oxygen species generation 2, 4
- Renal medullary ischemia from vasoconstriction and reduced medullary blood flow 2, 4
- Tubular epithelial and vascular endothelial injury 4
- Decreased glomerular filtration and renal hypoperfusion 2
Risk Factors Present
This patient likely had unrecognized risk factors 1, 8:
- Pre-existing renal impairment is the principal risk factor (10-fold increased risk when creatinine >2 mg/dL) 8, 6
- Possible diabetes mellitus or hypertension (common in TIA patients) 1, 6
- Age >60 years if applicable 1
Critical Clinical Pitfall
The major error here was likely failure to obtain pre-contrast creatinine and eGFR screening 1. Guidelines mandate that all patients with risk factors (age >60, diabetes, hypertension, suspected renal disease) must have serum creatinine measured and eGFR calculated before contrast administration 1. Had this been done, prophylactic measures could have been implemented 1, 8.
Management Implications
For this patient now 8:
- Monitor serum creatinine at 48-72 hours post-procedure (which is occurring now) 8
- Ensure adequate hydration if not contraindicated 8
- Discontinue nephrotoxic medications (NSAIDs, aminoglycosides if any) 1, 8
- Watch for volume overload, electrolyte disturbances, or uremic symptoms requiring dialysis 8
- Most cases are nonoliguric and self-limiting, with peak creatinine at 3-5 days 2, 6
Answer: B - Acute tubular necrosis