Diabetic Kidney Disease (DKD) can occur in approximately 30-40% of the population with type 1 or 2 diabetes mellitus around the world. In the pathogenesis and progression the Diabetic Kidney Disease (DKD), three fundamental axes are distinguished: hemodynamic, metabolic and inflammatory. The primary purpose of the review is to describe the role and mechanisms related to inflammation in the course of this disease. The pathophysiological mechanisms involved in the development and progression of DKD include different pathways present long before the clinical diagnosis of the disease. Inflammation is a complex mechanism where innate and acquired immunity play an important role, in addition to other factors such as oxidative stress and end products of glycation that in one way or another would be linked to this process of inflammation. We cannot forget the contribution in this axis of inflammation of the well-known aldosterone escape phenomenon. The blockade of the Mineralocorticoid Receptor (MRA) inactivates the action of aldosterone and prevents the genomic and non-genomic response from interacting with the receptor, thus decreasing the degree of inflammation and remodeling in the heart and kidney. Finally, there are many territories to explore in this fascinating universe of inflammation as a mechanism of kidney damage in diabetic patients. Current management of DKD with innovative interventions point to this multitarget approach.

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