When to Consider Cholesterol Emboli After Cardiac Catheterization
An 82-year-old hypertensive, diabetic man with Canadian Cardiovascular Society Grade III angina underwent cardiac catheterization after a grossly positive stress test while on optimal medical therapy. After some manipulation of coronary catheters through severe aortoiliac disease via transfemoral approach, he was shown to have severe three-vessel disease (including left main) and moderate left ventricular dysfunction. He was then admitted to the hospital for inpatient coronary artery bypass graft surgery. Table 1 shows inpatient biochemical information.
Table 1: Inpatient Biochemical Information
|
Pre-Angiography |
3 Days Post-Angiography |
6 Days Post-Angiography |
Glomerular Filtration Rate (GFR) (ml/min/1.73 m2) |
60 |
20 |
55 |
Blood Pressure |
140/70 |
135/80 |
144/80 |
Urine Sediment |
Bland |
Bland |
Bland |
Urine Output (ml/hr) |
50 |
40 |
50 |
Which of the following is the most likely cause of his kidney dysfunction?
Show Answer
The correct answer is: B. Contrast-induced nephropathy
Table 2 distinguishes between contrast-induced nephropathy and cholesterol emboli. Although this patient has risk factors for cholesterol emboli (for example, peripheral vascular disease, old age, and hypertension), answer A is incorrect because his GFR dropped by day 3 as opposed to an expected GFR drop days to weeks later. Also, there are no associated skin or eye findings described. Importantly, accelerated hypertension is not described in the patient's clinical course. Answer C is incorrect because patient had bland urine and no evidence of granular casts. There are no other supporting features to suggest that answer D is correct; there is no evidence of end organ malperfusion, and urine output did not decrease. Therefore, contrast-induced nephropathy is the most likely choice given the timing of onset and offset of decreased GFR.
Table 2: Contrast-Induced Nephropathy Versus Cholesterol Emboli
|
Contrast-Induced Nephropathy |
Cholesterol Emboli |
Pathophysiology |
Vasoconstriction; free radical injury to renal tubular cells; hypoxemia |
Plaque debris embolizes to small arteries |
Inflammatory Response |
N/A |
Increased erythrocyte sedimentation rate; decreased C3 and C4; eosinophilia |
Incidence of Renal Failure |
<1 to >20% |
1.4 to 1.9% |
Peripheral Manifestations |
N/A |
Accelerated hypertension; livedo reticularis; blue toe syndrome; eye findings |
Onset |
Peaks in 48-72 hrs;
may resolve 4-7 days |
Acute: 1-2 weeks
Sub-acute: weeks in “staircase pattern” |
Urine |
May be bland; may show acute tubular necrosis (granular casts) |
Bland +/- proteinuria |
References
- Kronzon I, Saric M. Cholesterol embolization syndrome. Circulation 2010;122:631-41.
- Kagan A, Sheikh-Hamad D. Contrast-induced kidney injury: focus on modifiable risk factors and prophylactic strategies. Clin Cardiol 2010;33:62-6.
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