Sunitinib-induced endocapillary proliferative glomerulonephritis with IgA2 deposit in addition to thrombotic microangiopathy: a case report.

IF 2.2 4区 医学 Q2 UROLOGY & NEPHROLOGY
Xin Zhang, Hui Wang, Jian Li, Fude Zhou, Minghui Zhao, Tao Su
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Abstract

Background: Sunitinib, a multi-targeted tyrosine kinase inhibitor, is used as a second-line therapy for gastrointestinal stromal tumors (GIST) resistant to imatinib. However, its impact on the vascular endothelial growth factor (VEGF) pathway can lead to significant toxicities, including hypertension and thrombotic microangiopathy (TMA).

Case presentation: This case report describes a unique instance of a patient with metastatic GIST who developed endocapillary proliferative glomerulonephritis (EPGN) with IgA2 deposits and TMA following sunitinib treatment. The patient presented with severe hypertension, nephrotic syndrome, and acute kidney injury. Renal biopsy confirmed the diagnosis, revealing IgA2 deposits, which are not commonly associated with TMA. Discontinuation of sunitinib led to a rapid improvement in renal function and proteinuria. The potential mechanisms underlying sunitinib-induced glomerular injury may involve the blockade of VEGFR-1, affecting immune cell recruitment and function, and the disruption of the nitric oxide and endothelin systems, leading to endothelial damage and immune dysregulation. Management of these toxicities requires a personalized approach, with options ranging from symptomatic relief to drug discontinuation. The use of endothelin receptor antagonists and other therapeutic alternatives for GIST management is discussed.

Conclusions: This case highlights the complex interplay between the therapeutic effects of sunitinib and its potential renal and cardiovascular toxicities, emphasizing the need for close monitoring and effective management strategies to optimize patient outcomes.

舒尼替尼诱发的内毛细血管增生性肾小球肾炎伴有IgA2沉积和血栓性微血管病:一份病例报告。
背景:舒尼替尼是一种多靶点酪氨酸激酶抑制剂,用于对伊马替尼耐药的胃肠道间质瘤(GIST)的二线治疗。然而,它对血管内皮生长因子(VEGF)通路的影响会导致严重的毒性,包括高血压和血栓性微血管病(TMA):本病例报告描述了一名转移性 GIST 患者在接受舒尼替尼治疗后出现伴有 IgA2 沉积和 TMA 的毛细血管内增生性肾小球肾炎(EPGN)的独特病例。患者出现严重高血压、肾病综合征和急性肾损伤。肾活检证实了诊断,发现了IgA2沉积物,而这种沉积物与TMA并不常见。停用舒尼替尼后,患者的肾功能和蛋白尿迅速改善。舒尼替尼诱发肾小球损伤的潜在机制可能包括阻断血管内皮生长因子受体-1(VEGFR-1),影响免疫细胞的募集和功能,以及破坏一氧化氮和内皮素系统,导致内皮损伤和免疫失调。对这些毒性的处理需要个性化的方法,可选择从缓解症状到停药等多种方案。本文讨论了如何使用内皮素受体拮抗剂和其他治疗方法来治疗 GIST:本病例突出了舒尼替尼的治疗效果与其潜在的肾脏和心血管毒性之间复杂的相互作用,强调了密切监测和有效管理策略的必要性,以优化患者的预后。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
BMC Nephrology
BMC Nephrology UROLOGY & NEPHROLOGY-
CiteScore
4.30
自引率
0.00%
发文量
375
审稿时长
3-8 weeks
期刊介绍: BMC Nephrology is an open access journal publishing original peer-reviewed research articles in all aspects of the prevention, diagnosis and management of kidney and associated disorders, as well as related molecular genetics, pathophysiology, and epidemiology.
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