Frontiers in oncology · 2026
Case Report: Glomerular microangiopathy and reversible renal toxicity during prolonged bevacizumab therapy in ovarian cancer.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Kwon Jungheon, Choe Misun, Paek Jin Hyuk, Park Woo Yeong, Jin Kyubok, Han Seungyeup, Cho Chi-Heum, Kim Yaerim
Аннотация
BACKGROUND: Bevacizumab, a VEGF-A inhibitor widely used in ovarian cancer, is associated with kidney adverse effects ranging from mild proteinuria to thrombotic microangiopathy (TMA). However, the longitudinal course, reversibility, and spectrum of kidney-limited injury remain under-characterized.
CASE REPORT: We describe three patients with ovarian cancer who developed proteinuria during prolonged bevacizumab therapy, including one with biopsy-proven kidney-limited glomerular microangiopathy. Proteinuria emerged after 6 to 12 months of exposure in all cases. Kidney function remained preserved throughout treatment. All three patients discontinued bevacizumab, after which proteinuria consistently improved. Two patients experienced complete resolution within 3 to 6 months, and one showed marked reduction to dipstick 1 plus by three months. Kidney biopsy in one case revealed double-contour basement membrane changes and subendothelial electron-dense deposits, confirming kidney-limited TMA without systemic microangiopathic findings.
CONCLUSION: These cases illustrate the characteristic time course of bevacizumab-induced kidney toxicity, highlight the reversibility of proteinuria following drug discontinuation, and demonstrate that bevacizumab can induce kidney-limited TMA in the absence of systemic microangiopathic features. Multidisciplinary management is essential to balance oncologic benefit with kidney safety.
CASE REPORT: We describe three patients with ovarian cancer who developed proteinuria during prolonged bevacizumab therapy, including one with biopsy-proven kidney-limited glomerular microangiopathy. Proteinuria emerged after 6 to 12 months of exposure in all cases. Kidney function remained preserved throughout treatment. All three patients discontinued bevacizumab, after which proteinuria consistently improved. Two patients experienced complete resolution within 3 to 6 months, and one showed marked reduction to dipstick 1 plus by three months. Kidney biopsy in one case revealed double-contour basement membrane changes and subendothelial electron-dense deposits, confirming kidney-limited TMA without systemic microangiopathic findings.
CONCLUSION: These cases illustrate the characteristic time course of bevacizumab-induced kidney toxicity, highlight the reversibility of proteinuria following drug discontinuation, and demonstrate that bevacizumab can induce kidney-limited TMA in the absence of systemic microangiopathic features. Multidisciplinary management is essential to balance oncologic benefit with kidney safety.