ArticleFrontiers in pharmacology2026
Multi-target tyrosine kinase inhibitor-associated renal thrombotic microangiopathy: a pooled analysis of 31 cases.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Renal toxicity during VEGF-pathway inhibition in cancer: a practical review of proteinuria, hypertension, and kidney-limited thrombotic microangiopathy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
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2 authors.
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Abstract
Background: Multi-target tyrosine kinase inhibitors (TKIs) are cornerstone therapies for solid malignancies, yet their association with renal thrombotic microangiopathy (TMA)-a severe, irreversible adverse event-remains incompletely defined. This study delineates TKI-associated renal TMA's clinical features, onset patterns, and outcomes. Methods: We systematically searched PubMed, Embase, Cochrane Library, and Web of Science for case reports/series of renal TMA linked to 7 multi-target TKIs (sunitinib, sorafenib, etc.) published through January 2026. Key data were extracted and analyzed descriptively. Results: Thirty-one cases were included (median age 62 years, 51.6% female). Common tumors: renal cell carcinoma (29.0%), thyroid cancer (16.1%), gastrointestinal stromal tumor (12.9%). Sunitinib was most implicated (48.4%). Median latency: 16 months (0.5-96 months); combination therapy shortened to 3.5 months. Dominant triad: hypertension (58.1%), AKI (77.4%), nephrotic proteinuria (67.9%); classic MAHA was uncommon. Kidney biopsy (87.1%) confirmed TMA. TKI discontinuation: 87.1% (6.5% dose reduction). Among evaluable patients, 90.0% improved, but 53.3% developed residual CKD and 10.0% ESRD. Conclusion: TKI-associated renal TMA presents as hypertension-proteinuria-AKI rather than classic hemolysis. Sunitinib confers highest risk, baseline hypertension is a key modifiable factor, and combination therapy accelerates onset. Lifelong monitoring and timely TKI discontinuation are critical, though residual CKD is common.
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