Increased glomerular size occurs in the presence of normal maturation, following unilateral nephrectomy in humans and animals, and in disease states such as diabetes mellitus. There are abnormalities in the circulating levels of GH in some diseases associated with increases in glomerular extracellular matrix and cell number, such as diabetes mellitus. The availability of transgenic mouse strains expressing elevated levels of GH provides an opportunity to study the renal effects of chronic hormone exposure. Progressive glomerulosclerosis leading to kidney failure develops in the GH transgenic mice. Mice transgenic for GH molecules containing mutations have also been examined in order to elucidate the domains of GH that may specifically code for genes responsible for glomerulosclerosis. We found an upregulation of mRNA for extracellular matrix components in the kidneys of the GH animals. This upregulation persisted late in the course of the disease.
