Performing Anticoagulation: A Puzzling Case of Cholesterol Embolization Syndrome

Figures

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  Figure 1.. Physical, magnetic resonance imaging (MRI), and pathological findings. Bluish reticulated patches were noted on the soles and tips of the toes (A), whereas T2-weighted HASTE diagnostic MRI (B) at a slightly more cephalic position from the renal arteries revealed an atherosclerotic plaque consisting of lipids (arrow) and fibrous (arrowhead) tissues in the abdominal aorta. Abnormal fluid-filled lesions (*), which may be ascribed to bilateral simple renal cysts, were also noted. Light microscopy of cutaneous biopsy sections revealed characteristic cholesterol clefts occluding the lumen of the arteriole (C, hematoxylin-eosin stain; the scale bar is indicated).

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  Figure 2.. Changes in renal parameter values, PT-INR, and percentage of eosinophils. The number “0” was designated as the point of the initial admission, and the patient was discharged on clinical day 51. There was a transient improvement in sCr levels, whereas the irreversible nature of severe renal failure eventually resulted in the initiation of chronic HD despite an increase in the dose of PSL (15 mg/day) combined with 9 sessions of LDL-A. Note that the amounts of urinary excreted proteins, β2MG, and NAG were almost completely constant during the observation period. The conversion of BUN (mg/dL) to urea (mmol/L) is accomplished by multiplying BUN by 0.357. To convert milligram per deciliter to micromole per liter for sCr, multiply by 88.4.