GH1 and type 1 diabetes mellitus: Taken together, GH excess associated with poorly controlled T1DM induces podocyte injury, characterized by podocyte hypertrophy, apoptosis, dedifferentiation of podocytes (epithelial–mesenchymal transition) and/or cross-linking of the basement membrane resulting in increased podocyte permeability to albumin and detachment of podocytes from the glomerular basement membrane (Fig. 1).