C5 inhibitor attenuates cholesterol crystal embolism–induced thrombotic microangiopathy and acute kidney injury

To the Editor, Cholesterol crystal embolism (CCE), an atherosclerotic complication, causes multi-organ microvascular obstruction (commonly involving kidneys) [1]. Thrombotic microangiopathy (TMA), characterized by microvascular endothelial injury, presents with consumptive thrombocytopenia, microangiopathic hemolytic anemia and multiorgan ischemia [2]. The complement pathway plays a central role in the pathogenesis of mutiple TMA subtypes. Studies have shown that cholesterol crystals trigger an inflammatory cascade by complement activation, causing endothelial injury and immunothrombosis [3, 4]. We present a CCE-mediated TMA-induced AKI case treated with a complement inhibitor, offering novel insights and therapeutic strategies for CCE. The case was a 67-year-old man with hypertension, hyperlipidemia, gout and extensive multiterritory atherosclerotic plaques, on irbesartan, amlodipine, terazosin, metoprolol, atorvastatin and febuxostat. Eight months previously, he had undergone coronary angiography followed by coronary artery bypass grafting for coronary artery disease with serum creatinine (Scr) levels fluctuating between 69.0 and 104.8 μmol/L. Dual antiplatelet therapy (aspirin 100 mg/day, clopidogrel 75 mg/day) was initiated. Three months before referral to our department, he presented with transient ischemic attack (TIA) by transiently altered consciousness, and then suffered kidney injury (Scr 238→360 μmol/L) and eosinophilia (1.02→1.34 × 109/L) over 3 months.