Abstract: Diabetic kidney disease （DKD） induces glomerular podocytes damages in multiple pathways， and podocyte lesions promote the progression of DKD. Mineralocorticoid regulates the salt and water concentration， fluid volume， and blood pressure by acting on mineralocorticoid receptor （MR）. MR expresses on intrinsic glomerular cells， such as podocytes， endothelial cells and mesangial cells. Its activation could change the structure and function of podocytes， damage the filtration barrier， and cause proteinuria. In the condition of diabetics， over-activation of MR will produce proteinuria and inflammation within kidney locally by upreglating oxidative stress， impairing ultrastructure， inhibiting autophagy and promoting apoptosis of podocytes. Blocking MR will prevent structural impairment， dysfunction and loss of podocytes， and even repair the filtration barrier. Here we review the pathophysiological mechanism of podocyte injury caused by diabetes， and the basic and clinical studies on the protection of podocytes with MR antagonist （MRA）， so as to provide a theoretical basis for MRA to ameliorate podocyte injury， reduce proteinuria， and improve kidney prognosis in the population with DKD.

Key words: diabetic mellitus, podocyte, mineralocorticoid receptor