NLRP3 inflammasome activation results in the release of pro-inflammatory interleukins. Several authors have demonstrated the presence of these interleukins in organs with inflammasome hyperactivation caused by intrinsic or extrinsic damage, for which kidney disease is not the exception; however, inflammasome activation has not been proved to be the cause in the light of an experimental model. Therefore, studying new therapies that focus on removing or inhibiting inflammasome components, both individually and together, is proposed in order to develop the hypothesis raised here. The involvement of inflammasome in human disease has incited efforts to identify potent and specific ways to interfere with NLRP3 activation in the context of auto-inflammatory diseases, including other diseases such as obesity, diabetes and hypertension.