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Published on: March 11, 2016
Surufatinib-induced renal thrombotic microangiopathy: first case report and review of literature
Wenjiao Zhu1, Wei Wang2, Yuanping Shi1
1Department of Endocrinology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Abstract:
Angiogenesis inhibitors such as tyrosine kinase inhibitors (TKIs) are common therapeutics currently used to treat oncologic disease. Surufatinib is a novel, small-molecule multiple receptor TKI approved by the National Medical Products Administration (NMPA) for the treatment of progressive, advanced, and well-differentiated pancreatic and extrapancreatic neuroendocrine tumours (NETs). Thrombotic microangiopathy (TMA) is a well-documented complication of TKIs targeting the VEGF-A/VEGFR2 signalling pathway. Here, we describe a 43-year-old female patient with biopsy-proven TMA and nephrotic syndrome due to surufatinib treatment for adenoid cystic carcinoma. Histological lesions included glomerular endothelial swelling, widening of subendothelial spaces, mesangiolysis, and double contour, which caused nephrotic proteinuria. Effective management was achieved by drug withdrawal and oral anti-hypertensive regents. The management of surufatinib-related nephrotoxicity without compromising its anticancer effects is challenging. Hypertension and proteinuria must be closely monitored during drug use to reduce or stop the dose in a timely manner before severe nephrotoxicity occurs.
Insights
Surufatinib, a tyrosine kinase inhibitor (TKI), can cause thrombotic microangiopathy (TMA) and nephrotic syndrome. Early detection and management, including dose adjustment, are crucial for patients undergoing TKI therapy.
Area of Science:
- Oncology
- Nephrology
- Pharmacology
Background:
- Tyrosine kinase inhibitors (TKIs) like surufatinib are vital in treating neuroendocrine tumors (NETs).
- Thrombotic microangiopathy (TMA) is a known complication of TKIs targeting the VEGF-A/VEGFR2 pathway.
- Surufatinib is approved for advanced pancreatic and extrapancreatic NETs.
Conclusions:
- Surufatinib can induce TMA and nephrotic syndrome, necessitating vigilant monitoring.
- Close monitoring of blood pressure and proteinuria is essential for timely dose modification or cessation of surufatinib.
- Balancing anticancer efficacy with managing surufatinib-induced nephrotoxicity is a clinical challenge.
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