A case report reveals thrombotic microangiopathy following chemotherapy in a child, indicating the need for vigilance in diagnosis.
Thrombotic microangiopathy (TMA) is a rare but life-threatening complication in patients with cancer and can be difficult to distinguish from other treatment-related toxicities. We report the case of an eight-year-old girl with metastatic Wilms’ tumor and a solitary kidney after left nephrectomy who developed biopsy-confirmed TMA following intensive multimodal therapy. She received multiple lines of chemotherapy, including actinomycin D, vincristine, cyclophosphamide, doxorubicin, and carboplatin, as well as radiotherapy to the bilateral lungs, nephrectomy bed, and whole abdomen. Several months into treatment, she developed progressive renal insufficiency with rising serum creatinine, microscopic hematuria, proteinuria, and subsequent extra-renal manifestations, including heart failure and new-onset seizures. Laboratory evaluation showed acute kidney injury, and renal biopsy demonstrated focal fibrin thrombi with mesangiolysis consistent with acute TMA, alongside mild acute tubular injury and non-specific immunofluorescence findings. In the absence of access to ADAMTS13 and complement genetic testing, chemotherapy-induced TMA, most likely related to cumulative exposure to carboplatin or doxorubicin in the context of prior radiotherapy, was considered the leading diagnosis. Withdrawal of chemotherapy was followed by partial renal recovery. This case highlights the need for a high index of suspicion for drug-induced TMA in pediatric oncology patients who develop new renal dysfunction and neurological or cardiac symptoms during or after exposure to multiple potentially endothelial-toxic agents. It also highlights the central role of renal biopsy in diagnosis and the importance of early recognition and treatment modification to preserve renal function, particularly in children with limited nephron reserve.
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Jamil et al. (2026) studied this question.
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