Pathophysiology of cisplatin-induced acute kidney injury.
Pathophysiology of cisplatin-induced acute kidney injury.
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DOI：
10.1155/2014/967826
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发表时间：
2014
影响因子：
--
通讯作者：
Edelstein CL
中科院分区：
文献类型：
--
作者：
Ozkok A;Edelstein CL
顺铂和其他铂衍生物是目前应用最广泛的化疗药物，用于治疗卵巢、头颈部和睾丸生殖细胞肿瘤等实体肿瘤。顺铂治疗的一个已知并发症是急性肾损伤(AKI)。顺铂的肾毒性作用是累积的和剂量依赖的，通常需要减少或停药。AKI的反复发作可能导致慢性肾脏疾病。顺铂诱导AKI的病理生理学涉及肾近端小管损伤、氧化应激、炎症和血管损伤。主要表现为急性肾小管坏死，近端肾小管也有细胞凋亡。肾脏中存在多种促炎细胞因子的激活和炎性细胞的浸润。抑制促炎细胞因子肿瘤坏死因子-α或IL-33或清除T细胞或肥大细胞对顺铂诱导的急性心肌梗死有保护作用。顺铂也会导致内皮细胞损伤。了解顺铂诱导AKI的发病机制对于开发预防AKI的辅助治疗、减少剂量减少或停药的必要性、降低患者的发病率和死亡率具有重要意义。
Cisplatin and other platinum derivatives are the most widely used chemotherapeutic agents to treat solid tumors including ovarian, head and neck, and testicular germ cell tumors. A known complication of cisplatin administration is acute kidney injury (AKI). The nephrotoxic effect of cisplatin is cumulative and dose-dependent and often necessitates dose reduction or withdrawal. Recurrent episodes of AKI may result in chronic kidney disease. The pathophysiology of cisplatin-induced AKI involves proximal tubular injury, oxidative stress, inflammation, and vascular injury in the kidney. There is predominantly acute tubular necrosis and also apoptosis in the proximal tubules. There is activation of multiple proinflammatory cytokines and infiltration of inflammatory cells in the kidney. Inhibition of the proinflammatory cytokines TNF-α or IL-33 or depletion of CD4+ T cells or mast cells protects against cisplatin-induced AKI. Cisplatin also causes endothelial cell injury. An understanding of the pathogenesis of cisplatin-induced AKI is important for the development of adjunctive therapies to prevent AKI, to lessen the need for dose decrease or drug withdrawal, and to lessen patient morbidity and mortality.
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DOI：
10.1124/jpet.103.060541
发表时间：
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影响因子：
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