Bevacizumab-induced thrombotic microangiopathy and nephrotic syndrome

Excerpt

A 64-year-old Japanese man with stage 4 adenocarcinoma of the lungs was referred to nephrology for proteinuria 1 month after initiating bevacizumab. The patient was alert and his blood pressure was 133/94 mmHg. There was pretibial edema on both legs. Hemoglobin level was 10.5 g/dL, platelet count was 10.8 × 10⁹/L, and the direct Coombs test was negative. Urinalysis showed 7.6 g/day of proteinuria and 50–99 erythrocytes per high-power field. Renal biopsy showed endotheliosis (Fig. 1), electron-dense deposits in subendothelial areas and foot process effacement (Fig. 2). Immunofluorescence microscopy showed IgA deposition mainly along capillary walls (Fig. 3). Bevacizumab was stopped, and the patient was followed up supportively. The proteinuria and hematuria gradually decreased 6 months thereafter. Bevacizumab, a humanized monoclonal antibody against vascular endothelial growth factor (VEGF), causes thrombotic microangiopathy by reducing VEGF signaling, and nephrotic syndrome due to foot process effacement [1‐4]. There is a case that reported electron-dense deposits decreased after the cessation of bevacizumab [5], but the relationship between anti-VEGF antibody and electron-dense deposit formation is unclear. Physicians should recognize these complications because they may progress to complete glomerulosclerosis without regression [3]. …