Department of Hematology, Kobe City Medical Center General Hospital, 2-1-1 Minami-machi, Minatojima, Chuo-ku, Kobe, Hyogo, 650-0047, Japan.
Department of Nephrology, Kobe City Medical Center General Hospital, Kobe, Hyogo, 650-0047, Japan.
BMC Nephrol. 2021 May 12;22(1):175. doi: 10.1186/s12882-021-02386-y.
Gemcitabine and cisplatin are chemotherapeutic agents used for treating multiple cancers, and these agents are sometimes used in combination. Drug-induced thrombotic microangiopathy (TMA) is a rare but potentially fatal complication. It typically presents as a systemic disease with the classical triad of hemolytic anemia, thrombocytopenia, and organ damage. In contrast to systemic TMA, cases of renal-limited TMA, defined as biopsy-proven renal TMA without the classical triad, have been reported with relatively good prognosis. Most cases of renal-limited TMA are associated with calcineurin inhibitors, and cases of drug-induced renal-limited TMA due to gemcitabine-dexamethasone-cisplatin therapy have been rarely reported.
A 43-year-old woman with lymphoma developed acute kidney injury with marked proteinuria, microhematuria, and abnormal urinary casts after receiving one cycle of gemcitabine-dexamethasone-cisplatin therapy. Although she did not show hemolytic anemia and thrombocytopenia, renal biopsy showed diffuse injury to the glomerular endothelial cells, supporting the diagnosis of renal-limited TMA. Her condition improved only with the cessation of gemcitabine and cisplatin treatment. She received another chemotherapy without gemcitabine and platinum agents, and no recurrence of renal-limited TMA was observed.
Drug-induced TMA occurs early after gemcitabine and cisplatin use in renal-limited form and is reversible when detected and managed in a timely manner. Urinalysis, which is simple and inexpensive and can be easily performed, is a beneficial screening tool for early-onset drug-induced TMA among patients who receive gemcitabine-dexamethasone-cisplatin therapy.
吉西他滨和顺铂是用于治疗多种癌症的化疗药物，这些药物有时联合使用。药物诱导的血栓性微血管病（TMA）是一种罕见但潜在致命的并发症。它通常表现为一种全身性疾病，具有溶血性贫血、血小板减少和器官损伤的典型三联征。与全身性 TMA 相反，肾局限性 TMA 的病例，即活检证实的无典型三联征的肾 TMA，已被报道具有相对较好的预后。大多数肾局限性 TMA 与钙调神经磷酸酶抑制剂有关，而由于吉西他滨-地塞米松-顺铂治疗引起的药物诱导的肾局限性 TMA 病例则很少见。
一名 43 岁女性患有淋巴瘤，在接受一个周期的吉西他滨-地塞米松-顺铂治疗后，出现急性肾损伤，伴有明显蛋白尿、镜下血尿和异常尿铸型。虽然她没有表现出溶血性贫血和血小板减少，但肾活检显示肾小球内皮细胞弥漫性损伤，支持肾局限性 TMA 的诊断。仅停止使用吉西他滨和顺铂治疗，她的病情才有所改善。她接受了另一种不含吉西他滨和铂类药物的化疗，未观察到肾局限性 TMA 复发。
在吉西他滨和顺铂使用后早期发生药物诱导的 TMA，呈肾局限性表现，及时发现和处理可逆转。尿分析简单、廉价且易于进行，是接受吉西他滨-地塞米松-顺铂治疗的患者中早期药物诱导 TMA 的有益筛查工具。
