Pegylated Liposomal Doxorubicin Causes Kidney-limited Thrombotic Microangiopathy

医学 血栓性微血管病 阿霉素 脂质体 微血管病 泌尿科 内科学 药理学 化疗 内分泌学 糖尿病 疾病 材料科学 纳米技术
作者
Ilya Glezerman,Steven Salvatore,William D. Tap,Ciara M. Kelly,C Ornelas,Attiya Shaikh
出处
期刊:American Journal of Kidney Diseases [Elsevier]
标识
DOI:10.1053/j.ajkd.2023.08.014
摘要

A definite causal link between pegylated liposomal doxorubicin (PLD) and kidney-limited thrombotic microangiopathy (TMA) remains unestablished. Here, we report 2 cases of PLD-induced kidney-limited TMA, 1 in a patient with myxofibrosarcoma and the other in a patient with liposarcoma. The 2 patients received a high cumulative dose of PLD, and both presented with a rise in serum creatinine and proteinuria. Kidney biopsy revealed TMA with chronic mesangiolysis and capillary wall double contouring. Neither patient had concomitant exposure to TMA-causing drugs, such as gemcitabine, anti–vascular endothelial growth factor agents, or mammalian target of rapamycin inhibitors. The work-up for secondary causes of TMA was negative in both patients. The cessation of PLD therapy led to improvement or stabilization in serum creatinine and proteinuria in both patients. These 2 cases provide a clear causal link between PLD and kidney-limited TMA. The high cumulative dose of PLD increases the risk of kidney TMA. Early recognition of PLD-induced kidney TMA can lead to timely cessation of PLD therapy and potentially preserve kidney function. A definite causal link between pegylated liposomal doxorubicin (PLD) and kidney-limited thrombotic microangiopathy (TMA) remains unestablished. Here, we report 2 cases of PLD-induced kidney-limited TMA, 1 in a patient with myxofibrosarcoma and the other in a patient with liposarcoma. The 2 patients received a high cumulative dose of PLD, and both presented with a rise in serum creatinine and proteinuria. Kidney biopsy revealed TMA with chronic mesangiolysis and capillary wall double contouring. Neither patient had concomitant exposure to TMA-causing drugs, such as gemcitabine, anti–vascular endothelial growth factor agents, or mammalian target of rapamycin inhibitors. The work-up for secondary causes of TMA was negative in both patients. The cessation of PLD therapy led to improvement or stabilization in serum creatinine and proteinuria in both patients. These 2 cases provide a clear causal link between PLD and kidney-limited TMA. The high cumulative dose of PLD increases the risk of kidney TMA. Early recognition of PLD-induced kidney TMA can lead to timely cessation of PLD therapy and potentially preserve kidney function.
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