摘要该文报道1例罕见的卡非佐米（carfilzomib，CFZ）诱发的血栓性微血管病（thrombotic microangiopathy，TMA）病例。患者男性，56岁，诊断为多发性骨髓瘤，接受CFZ化疗16个月后出现急性肾损伤（无尿）、重度贫血及血小板减少。肾活检证实TMA样改变，排除其他因素导致的TMA后确诊CFZ诱发的TMA。治疗上采用补体C5抑制剂（依库珠单抗）联合小剂量糖皮质激素。经上述治疗10 d后，肾功能完全恢复（血肌酐由峰值935 μmol/L降至基线80 μmol/L），贫血及血小板减少亦显著改善。文献复习提示，CFZ诱发的TMA的发病可能与补体旁路途径过度激活及相关基因（如补体H因子、补体I因子）变异有关。CFZ诱发的TMA是CFZ治疗中一种罕见但严重的并发症，临床医师需高度警惕，一旦怀疑，应立即停药。早期给予补体C5抑制剂（如依库珠单抗）靶向治疗，可有效阻断CFZ诱发的TMA的病理进程，改善患者预后。建议对疑似患者进行补体活性检测及基因筛查以指导治疗。

abstractsThis paper describes a rare case of carfilzomib (CFZ)-induced thrombotic microangiopathy (TMA). A 56-year-old man with multiple myeloma developed anuric acute kidney injury, severe anemia, and thrombocytopenia after 16 months of CFZ therapy. Renal biopsy demonstrated TMA-like changes. After exclusion of other causes, CFZ-induced TMA was diagnosed. The patient was treated with complement C5 inhibitor (eculizumab) combined with low dose of glucocorticoids. After 10 days of this combination therapy, renal function recovered completely (serum creatinine decreased from a peak of 935 μmol/L to a baseline of 80 μmol/L), and anemia and thrombocytopenia were also significantly improved. Literature review suggests that the pathogenesis of CFZ-induced TMA may be associated with excessive activation of the alternative complement pathway and variations in related genes (e.g., complement factor H and complement factor I). CFZ-induced TMA is a rare but severe complication during CFZ treatment, and clinicians must be highly vigilant. CFZ should be discontinued immediately upon suspicion of CFZ-induced TMA. Early targeted therapy with complement C5 inhibitors (e.g., eculizumab) can effectively block the pathological process of CFZ-induced TMA and improve prognosis. It is recommended to perform complement activity testing and genetic screening in suspected patients to guide treatment.