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Diagnosis: Thrombotic Micronagipathy and Secondary FSGS

Thrombotic microangiopathy (TMA) is an complication of oncologic therapy. Cancer-related causes of renal endothelial cell damage include cytotoxic chemotherapies, radiation given for myeloablation, and direct involvement of renal vasculature by tumor cells. Another class of therapeutic agents that has been implicated in TMA is the vascular endothelial growth factor (VEGF) pathway inhibitors, including the anti-VEGF monoclonal antibody bevacizumab and the VEGF receptor tyrosine kinase inhibitor sunitinib. These TMAs have been termed type II cancer drug-induced TMA and are distinguished from those associated with some cytotoxic chemotherapies (ie, type I) in that they are not dose dependent and patients are more likely to demonstrate some recovery of kidney function. Determination of the cause of TMA in oncologic patients often presents a significant challenge because patients frequently receive multiple chemotherapeutic agents simultaneously and clinicopathologic features often demonstrate substantial overlap, regardless of cause (Miller AJ, et al. Chronic Microangiopathy Due to DCR-MYC, a Myc-Targeted Short Interfering RNA. Am J Kidney Dis. 2020;75:513-516. [PubMed link]).

In our case, although recent thrombi were not evident, there is remodeling of the glomerular basement membranes, with some double contours and multiple hyaline accumulations, some of them intracapillary ("focal and segmental hyalinosis"). The patient was receiving sunitinib. Three months after stopping this medication, the patient continued with impaired kidney function and nephrotic proteinuria. It is possible that the extensive chronic changes were already advanced.

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