舒尼替尼是一种多靶点酪氨酸激酶抑制剂，用作对伊马替尼耐药的胃肠道间质瘤（GIST）的二线疗法。然而，它对血管内皮生长因子 (VEGF) 通路的影响可能导致显着的毒性，包括高血压和血栓性微血管病 (TMA)。本病例报告描述了一名患有毛细血管内增生性肾小球肾炎 (EPGN) 的转移性胃肠道间质瘤患者的独特实例舒尼替尼治疗后出现 IgA2 沉积和 TMA。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，显示 IgA2 沉积，这通常与 TMA 无关。停用舒尼替尼导致肾功能和蛋白尿迅速改善。舒尼替尼诱导肾小球损伤的潜在机制可能涉及阻断 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。这些毒性的管理需要采取个性化的方法，选择范围从缓解症状到停药。讨论了内皮素受体拮抗剂和其他治疗替代方案在 GIST 治疗中的使用。该病例强调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，强调需要密切监测和有效的管理策略以优化患者的治疗结果.© 2024。作者。

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).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.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.© 2024. The Author(s).