Acute Tubular Necrosis from Contrast-Induced Nephropathy
The most likely mechanism for renal impairment in this patient is acute tubular necrosis (ATN) secondary to contrast-induced nephropathy (CIN), given the temporal relationship of CT brain with contrast 2 days prior and the markedly elevated creatinine (378 μmol/L) with disproportionately elevated urea (30.4 mmol/L).
Clinical Reasoning
Temporal Relationship Points to Contrast Nephropathy
The classic presentation of CIN is an asymptomatic increase in serum creatinine 1-5 days following intravascular contrast injection, which precisely matches this patient's timeline of CT brain with contrast 2 days ago 1, 2. The patient's creatinine of 378 μmol/L represents a dramatic rise from the upper limit of normal (115 μmol/L), consistent with acute kidney injury rather than chronic renal disease 3.
Mechanism: Direct Tubular Toxicity
Contrast-induced nephropathy causes ATN through two primary mechanisms: renal vasoconstriction and direct tubular cell injury 2. The contrast agent causes direct tubular toxicity, leading to tubular epithelial cell damage and necrosis, which is the pathophysiologic hallmark of ATN 1, 2.
Why Not Pre-renal Azotemia?
Pre-renal azotemia is excluded by the clinical presentation. The patient has normal vital signs (BP 130/70 mmHg, HR 76/min) without evidence of volume depletion, hypotension, or decreased renal perfusion 4. While the BUN:creatinine ratio appears elevated, this is more consistent with the catabolic state and tubular dysfunction of ATN rather than true pre-renal physiology 2.
Why Not Acute Interstitial Nephritis?
Acute interstitial nephritis typically presents with fever, rash, eosinophilia, and pyuria—none of which are mentioned in this case 4. The temporal relationship with contrast exposure and absence of these systemic features make AIN unlikely.
Why Not Acute Glomerular Nephritis?
Acute glomerulonephritis would typically present with hematuria, proteinuria, edema, and hypertension, with a more gradual onset 4. The acute presentation following contrast exposure without these features makes glomerulonephritis improbable.
Risk Factors Present
Vascular Risk Factors
This patient has vascular risk factors (possible TIA) that increase CIN risk substantially 4. Patients with underlying cardiovascular disease have significantly higher risk of CIN, with incidence reaching up to 20% in selected patient subsets compared to 0.6-2.3% in the general population 3.
Baseline Renal Function Considerations
The most critical risk factor for CIN is pre-existing renal impairment, with risk increasing 5- to 10-fold when baseline serum creatinine exceeds 1.5 mg/dL (133 μmol/L) 4, 2. Even if this patient had mild baseline renal dysfunction (which we cannot determine from the current data), this would dramatically increase CIN risk 5.
Clinical Implications
Prognosis and Mortality
Patients who develop CIN after contrast exposure sustain increased short- and long-term mortality, whether or not chronic kidney disease was present prior to contrast exposure 1. This diminished survival occurs both in patients whose acute renal failure is not severe enough to require dialysis and in those requiring dialysis 1.
Prevention Missed Opportunity
The guidelines recommend checking renal function prior to contrast administration in patients with risk factors including age over 60 years, history of vascular disease, and suspected cerebrovascular disease 4. Aggressive pre-study hydration along with selective use of low-osmolar contrast media can significantly reduce CIN risk 2, 6.
Common Pitfalls
Do not dismiss elevated creatinine as chronic kidney disease without considering recent contrast exposure. The temporal relationship is the critical diagnostic clue—CIN typically manifests 48-72 hours after contrast administration 3.
Do not delay supportive management while awaiting additional testing. Treatment is limited to supportive measures including hydration and avoidance of further nephrotoxic agents, as there are no specific therapies for established CIN 1, 2.
Do not administer additional contrast studies in the acute phase. Further contrast exposure will worsen tubular injury and should be avoided until renal function recovers 4.