PDPN and preeclampsia: Although we did not study the direct cause‐effect relationship between CuZn SOD function and podocyte/nephrin loss, using a low‐oxygen culture condition or cells treated with CoCl2 as a model of oxidative stress condition in human AB 8/13 podocytes we observed an interesting phenomenon that hypoxia (oxidative stress) downregulates or induces dislocation of nephrin and podoplanin from foot‐process area to cytosol in podocytes, which is associated with loss of CuZn‐SOD expression in podocytes and mimics what we found in podocytes‐derived from patients with preeclampsia.