CKD Induced by Cholesterol Crystal Embolization (CCE)

Introduction: CCE typically impacts individuals with widespread erosive atherosclerosis. This occurs when fragments of atherosclerotic plaques detach and travel to distant locations, causing the partial or complete blockage of numerous small arteries, including glomerular arterioles, leading to ischemia in affected tissues or organs. Case Description: 68-year-old man with CAD post-left heart catheterization with stent placement 4w ago, CKD3, HTN, DM and Afib presented to the ED with fatigue and melena for 3 days. His meds include amlodipine, metformin, aspirin, Plavix and Eliquis. In the ED, he was stable and labs with slight leukocytosis, Cr 3.8, K 5.8, BUN 71, and lactate 2.8. He received 1uPRBC, and a positive FOBT with general surgery consultation for GI bleed workup. Initially, his AKI was thought to be prerenal due to GI bleed from anticoagulation intolerance. However, EGD and colonoscopy were benign. Eliquis was held. He responded well to transfusion and received maintenance IVF. Repeat labs showed improved BUN but Cr at 5.3 by day 5. A repeat UA on day 3 revealed hyaline and granular casts. Despite good urine output, Cr levels did not improve. Renal US showed a slightly atrophic right kidney. Autoimmune workup and complement levels were normal. A renal biopsy of the right kidney showed light microscopy findings consistent with tubular injury and cholesterol emboli in vessels. Electron microscopy revealed mild thickening of the glomerular basement membrane and focal effacement of podocyte foot processes. The IF study was negative. With a stable chonic renal injury and HPE findings, he was diagnosed with CCE. Discussion: CCE requires suspicion, especially with AKI, hypereosinophilia, livedo reticularis, or blue toe syndrome in elderly men with atherosclerosis or recent vascular interventions like cardiac cath, with fever, weight loss, anorexia, fatigue, and myalgias. Labs may show elevated WBCs, ESR, CRP, reduced C3/C4, anemia and low Plts. Hypereosinophilia is seen in 80% of cases, mediated by cytokines potentially IL 5 from vascular endothelium. Biopsy, preferably of affected skin or muscles remains the gold standard. Treatment focuses on supportive care for end-organ damage and preventing recurrent cholesterol embolization episodes. Addressing atherosclerosis risk factors like smoking, hypertension, and cholesterol is crucial. Mention on statin, antiplatelets and revascularization therapy is made.