Alterations and injury to glomerular podocytes play a key role in the initiation and
progression of diabetic kidney disease (DKD). Multiple factors in diabetes cause
abnormalities in podocyte signaling that lead to podocyte foot process effacement,
hypertrophy, detachment, loss, and death. Alterations in insulin action and mammalian
target of rapamycin activation have been well documented to lead to pathology. Reduced
insulin action directly leads to albuminuria, increased glomerular matrix accumulation …