Focal segmental glomerulosclerosis lesion associated with inhibition of tyrosine kinases by lenvatinib: a case report

被引:18
作者
Furuto, Yoshitaka [1 ]
Hashimoto, Hirotsugu [2 ]
Namikawa, Akio [1 ]
Outi, Haruki [1 ]
Takahashi, Hiroko [1 ]
Horiuti, Hajime [2 ]
Honda, Kazuho [3 ]
Shibuya, Yuko [1 ]
机构
[1] NTT Med Ctr Tokyo, Dept Hypertens & Nephrol, Shinagawa Ku, 5-9-22 Higasi Gotanda, Tokyo 1418625, Japan
[2] NTT Med Ctr Tokyo, Dept Diagnost Pathol, Shinagawa Ku, 5-9-22 Higasi Gotanda, Tokyo 1418625, Japan
[3] Showa Univ Hosp, Dept Microscop Anat, Shinagawa Ku, 1-5-8 Hatanodai, Tokyo 1428666, Japan
来源
BMC NEPHROLOGY | 2018年 / 19卷
基金
日本学术振兴会;
关键词
Lenvatinib; Tyrosine kinase inhibitors; Focal segmental glomerulosclerosis; Thyroid cancer; RENAL-CELL CARCINOMA; ANTI-VEGF THERAPY; GROWTH-FACTOR VEGF; THROMBOTIC MICROANGIOPATHY; NEPHROTIC SYNDROME; C-MIP; ANTITUMOR ACTIVITIES; KIDNEY-DISEASES; CANCER-PATIENTS; THYROID-CANCER;
D O I
10.1186/s12882-018-1074-3
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Background: Lenvatinib is a tyrosine kinase inhibitor with novel binding ability. It is considered the standard of care for metastatic thyroid cancer; moreover, whether it is indicated for other malignant tumors has been examined. Lenvatinib increases the risk of kidney injury in some patients. In comparison with sorafenib, which is a conventional tyrosine kinase inhibitor (TKI), lenvatinib results in more side effects, including hypertension and proteinuria. We describe a case of secondary focal segmental glomerulosclerosis (FSGS) that developed following treatment of metastatic thyroid cancer with lenvatinib and reviewed the mechanisms of renal impairment. Case presentation: We describe a patient with metastatic thyroid cancer who developed hypertension, nephrotic syndrome, and acute kidney injury after 3months of lenvatinib treatment. Renal biopsy results revealed that 7 of 16 glomeruli indicated complete hyalinization, and that the glomeruli with incomplete hyalinization showed FSGS due to a vascular endothelial disorder and podocyte damage, which seemed to have been induced by lenvatinib treatment. These findings were similar to those of renal impairment treated with conventional TKIs. Although lenvatinib treatment was discontinued, up to 15 months were required to achieve remission of proteinuria, thus leading to chronic kidney disease with hyalinized lesions. Conclusions: To the best of our knowledge, this is the first reported case of secondary FSGS by lenvatinib treatment. Renal impairment treated with TKIs is commonly associated with minimal change nephrotic syndrome/FSGS findings, and it is suggested that renal involvement with TKI is different from that with the vascular endothelial growth factor ligand. Overexpression of c-mip due to TKI causes disorders such as podocyte dysregulation and promotion of apoptosis, which cause FSGS. Lenvatinib may result in FSGS by a similar mechanism with another TKI and could cause irreversible renal impairment; therefore caution must be used. It is essential to monitor blood pressure, urinary findings, and the renal function.
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页数:9
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