| Literature DB >> 28774729 |
Rania Kheder El-Fekih1, Clément Deltombe2, Hassan Izzedine3.
Abstract
Thrombotic microangiopathy (TMA) is a group of disorders characterized by mechanical hemolytic anemia with thrombocytopenia and an ischemic organic lesion of variable and potentially fatal importance affecting mostly the kidneys and the brain with histologically a disseminated and occlusive microvasculopathy. The incidence of TMA represents 15% of acute kidney failure in oncological setting, largely due to the introduction of anti-angiogenic agents over the past decade. It may be more rarely related to cancer itself. The iatrogenic TMA can be classified into 2 types: The type I, secondary to chemotherapy (mitomycinC, gemcitabine), exposes to a chronic dose-dependent renal injury as well as an increase in morbidity and mortality; iatrogenic type II, secondary to anti-angiogenic agents', results in a dose-independent renal involvement and renal functional recovery is usual when the drug is discontinued. There is no randomized controlled trial to establish EBM-type management in TMA support. However, complement activation pathways and regulatory factors analyses allowed us to understand the mechanisms of endothelial lesions. As a result, the current trend includes the use of immunosuppressive agents in recurrent or plasmapheresis-refractory MAT.Entities:
Keywords: Anti-VEGF; Gemcitabine; Greffe de cellules souches hématopoïétiques; Hematopoietic stem cell transplant; Microangiopathie thrombotique; Mitomycin C; Mitomycine C; Plasmapheresis; Plasmaphérèse; Thrombotic microangiopathy
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Year: 2017 PMID: 28774729 DOI: 10.1016/j.nephro.2017.01.023
Source DB: PubMed Journal: Nephrol Ther ISSN: 1769-7255 Impact factor: 0.722