Loss of podocytes promotes glomerulosclerosis, but whether this results from a continued
primary insult or a secondary mechanism triggered by the initial loss of podocytes is
unknown. We generated chimeric mice in which only a subpopulation of podocytes
expressed hCD25, which is the receptor for the immunotoxin LMB2. In addition, genetic
labeling of hCD25-negative cells with human placental alkaline phosphatase allowed the
study of these two distinct podocyte populations. Administration of LMB2 did not cause …