The exact mechanisms by which growth hormone (GH) damages the kidney induci
ng diabetic nephropathy has not yet been elucidated. Recently, it has been
shown that transferrin has the same diabetogenic effects of GH, being its m
ediator. Transferrin was studied using immunohistochemistry and immunoelect
ron microscopy in cases of early diabetic nephropathy, and in controls. Tra
nsferrin was only found in diabetic cases in podocytes and Bowman's capsule
cells, but also in the tubular cells of both diabetic and non-diabetic con
trols. Immune-electron microscopy for the presence of transferrin showed po
sitive signals in the cytoplasm of diabetic podocytes, but not in pedicels.
This selective deposition was associated with signs of organelle and cytos
keleton damage. On the basis of previous evidence and present glomerular fi
ndings, these results suggest an indirect diabetogenic effect on the kidney
by GH mediated through transferrin.