The regulatory role of IFN-γ in the production of renal localized angiotensinogen leads to overactivation of the AngII-renin-angiotensin aldosterone system, resulting in increased aldosterone production, water and sodium reabsorption, and ultimately hypertension.234–238 This cascade of events can cause damage to renal capillary endothelial cells and contribute to the development of renal atherosclerosis. This evidence concerns the gene AGT and renal artery atheroma.