Oliveira-Silva Catarina, Viana Johanna, Coelho Claudia, Silva Roberto, Falcão Luís, Rocha Joana, Ribeiro Bárbara
Nephrology Department, Unidade Local de Saúde de Braga, Braga, Portugal.
Pathology Department, Unidade Local de Saúde de São João, Porto, Portugal.
Eur J Case Rep Intern Med. 2025 Aug 19;12(9):005565. doi: 10.12890/2025_005565. eCollection 2025.
Bevacizumab is a monoclonal antibody that targets vascular endothelial growth factor (VEGF) and is widely used in oncology for its anti-angiogenic properties. However, VEGF inhibition may result in significant nephrotoxicity, including thrombotic microangiopathy (TMA). While systemic TMA is well-described, isolated renal-limited TMA remains under recognised.
We present a 46-year-old woman with WHO grade IV IDH-wildtype EGFR-amplified gliosarcoma. She received second-line treatment with bevacizumab and, after 12 months of therapy, developed progressive hypertension and nephrotic-range proteinuria up to 6.2 g/day, with normal renal function and without anaemia or thrombocytopenia. A kidney biopsy revealed glomerular microangiopathy, and a diagnosis of bevacizumab-associated renal-limited TMA was established. Given the stability of the intracranial disease, the drug was discontinued with complete resolution of proteinuria after seven months.
Anti-VEGF therapy causes renal TMA and may present with nephrotic-range proteinuria associated with a pattern of glomerular microangiopathy. Recognising anti-VEGF-associated nephrotoxicity is essential in the differential diagnosis of proteinuria in cancer patients, and kidney biopsy is fundamental for guiding clinical decisions. Drug cessation led to the complete resolution of proteinuria.
Bevacizumab can cause renal-limited thrombotic microangiopathy and may present with nephrotic-range proteinuria, without renal dysfunction.Kidney biopsy is essential to distinguish drug-induced thrombotic microangiopathy from malignancy-associated nephropathies in cancer patients.Early recognition and drug discontinuation can lead to complete proteinuria resolution.
贝伐单抗是一种靶向血管内皮生长因子（VEGF）的单克隆抗体，因其抗血管生成特性而广泛应用于肿瘤学领域。然而，VEGF抑制可能导致显著的肾毒性，包括血栓性微血管病（TMA）。虽然全身性TMA已有详细描述，但孤立性肾局限性TMA仍未得到充分认识。
我们报告一名46岁患有世界卫生组织IV级异柠檬酸脱氢酶野生型、表皮生长因子受体扩增的胶质肉瘤女性患者。她接受了贝伐单抗二线治疗，治疗12个月后出现进行性高血压和高达6.2克/天的肾病范围蛋白尿，肾功能正常，无贫血或血小板减少。肾脏活检显示肾小球微血管病，确诊为贝伐单抗相关性肾局限性TMA。鉴于颅内疾病稳定，停药7个月后蛋白尿完全消退。
抗VEGF治疗可导致肾TMA，并可能表现为与肾小球微血管病模式相关的肾病范围蛋白尿。认识到抗VEGF相关肾毒性对于癌症患者蛋白尿的鉴别诊断至关重要，肾脏活检是指导临床决策的基础。停药导致蛋白尿完全消退。
贝伐单抗可导致肾局限性血栓性微血管病，并可能表现为肾病范围蛋白尿，而无肾功能障碍。肾脏活检对于区分癌症患者药物性血栓性微血管病与恶性肿瘤相关性肾病至关重要。早期识别和停药可导致蛋白尿完全消退。
