NLRP3 and chronic kidney disease: Some of the pathophysiological mechanisms known to contribute to CKD progression include the overactivity of the renin-angiotensin-aldosterone system (RAAS), with consequent increase in the biological effects of Angiotensin II (AII), and the activation of local innate and adaptive immune responses which trigger the production of proinflammatory mediators, leukocyte recruitment, and ECM synthesis [4–9].