A 63-year-old man with a history of smoking, obesity, arterial hypertension, diabetes mellitus, and previous deep venous thrombosis (DVT) in the left leg was admitted to the emergency department due to myocardial infarction. Upon admission, laboratory tests revealed serum creatinine of 2.3 mg/dL (normal, 0.9–1.3 mg/dL) and urea of 79 mg/dL (normal, 10–40 mg/dL). Coronary angiography revealed severe and complex lesions in all three arteries. Surgical myocardial revascularization was performed without complications. The patient was discharged on the 19th postoperative day in satisfactory condition with a creatinine of 1.93 mg/dL. However, he presented to the hospital again 7 days after discharge, complaining of chest pain and dyspnea. Chest angiotomography revealed a right-sided pulmonary embolism, while venous Doppler imaging of the lower limbs showed no signs of a recent DVT. The patient was started on full anticoagulation with unfractionated heparin, later transitioning to apixaban. Hematological investigations for hypercoagulable disorders yielded negative results. During outpatient follow-up, 24-hour proteinuria was 264 mg/day and creatinine level rose to 3.53 mg/dL. Doppler of the renal arteries showed abdominal aortic atheromatosis without significant stenosis, with a fusiform aneurysmal dilation in the infrarenal segment measuring approximately 8.4 cm in length and 4.4 cm in diameter, and normal kidney size. Despite the patient’s history of hypertension, retinal imaging was normal. Due to the continuous and unexplained progressive deterioration of renal function (creatinine level, 4.19 mg/dL), a kidney biopsy was performed at the 5-month follow-up, which showed cholesterol crystal embolism (CCE) of the renal arterioles (
Fig. 1). The kidney biopsy also showed slight thickening of the tunica intima in some arteries. The patient had stable kidney function and did not require renal replacement therapy during a year follow-up (
Fig. 2).
CCE may occur after intra-arterial procedures and is rarely spontaneous. Cholesterol crystals and atheroma debris embolize from proximal large arteries to distal small arteries, mechanically obstructing vascular beds and leading to an inflammatory response, leukocyte infiltration, and complement activation in the target organs. CCE is a multisystemic disease of the brain, skin, eyes, gastrointestinal tract, and retinal vessels. Kidney damage (64%–74% of CCE cases) can manifest in acute, subacute, or chronic forms, with approximately 36% of patients requiring early dialysis. The first form clinically manifests as acute kidney injury, microscopic hematuria, eosinophilia, and minimal proteinuria, while the chronic form most often presents as continuous and unexplained progressive deterioration of renal function; therefore, kidney biopsy is essential in these cases. Because of the limited therapeutic options, CCE has poor long-term renal outcomes, with renal function recovery in only 25% of cases.