Based on its temporal relationship with the cessation of
immunosuppressive therapy, NS was suggested to be a
glomerular manifestation of cGVHD [18]. Murine models of
cGVHD have demonstrated membranous changes in the host
kidney after donor lymphocyte infusion [19]. Both direct
mesangial damage and massive immune complex deposition
might be involved and followed by the release of cytokines in
a murine model of cGVHD [20]. Dysregulation of immune
cells (both T and B cells) and cytokines is found to be involved
in the evolution of NS, but these data are still limited.