Podocyte loss contributes to the development of glomerulosclerosis. Although podocyte
detachment has been recognized as a new mechanism of podocyte loss in glomerular
diseases, its time course and relationship to disease activity are not known. Urinary
excretion of viable podocytes was quantified in two models of transient glomerular injury, ie,
rats with puromycin aminonucleoside-induced nephrosis (PAN) and mesangioproliferative
nephropathy (anti-Thy 1.1 nephritis model), as well as in a model of continuous glomerular …