Imatinib-induced podocytopathies in a patient with gastrointestinal stromal tumor

Figures & data

Figure 1. (A) Histological examination of the gastrointestinal stromal tumor (H&E staining × 200). (B, C) Electron microscopy revealed diffuse podocyte foot process effacement, which was considered as podocytopathies (minimal change disease or underlying focal segmental glomerulosclerosis) with acute tubulointerstitial injury (magnification × 2000). (D) Immunofluorescence showing no immune complex deposition (IgG-A-M, C3, C1q).

Figure 2. Significant increase in proteinuria and creatinine during imatinib treatment (arrows). The rapid decrease in proteinuria and creatinine after the stop of imatinib and use of glucocorticoids (arrows).

Figure 3. The high expression of c-mip in podocytes blocks the Fyn-Nephrin protein signaling pathway, preventing Nephrin from recruiting PIK3, NcK, and N-wasp. Nephrin is unable to phosphorylate and activate Akt, and podocytes cannot participate in normal filtration barrier and secretion of vascular endothelial growth factor (VEGF).

Data availability statement

All data are included in the manuscript.