Renal inflammation is a universal response to infectious and noninfectious triggers. Sensors of the innate immune system, such as Toll-like receptors or RIG-like receptors, provide danger recognition platforms on renal cells that integrate and translate the diverse triggers of renal inflammation by inducing cell activation and the secretion of proinflammatory cytokines and chemokines. As a new entry, the inflammasome-forming NLR genes integrate various danger signals into caspase-1-activating platforms that regulate the processing and secretion of pro-IL-1β and pro-IL-18 into the mature and active cytokines. Accumulating data now document a role for the NLRP3 inflammasome and IL-1β/IL-18 in many diseases, including atherosclerosis, diabetes, amyloidosis, malaria, crystal-related diseases, and other autoinflammatory disorders, identifying this innate immune pathway as an attractive therapeutic target. Here we review the current knowledge regarding inflammasome signaling and outline existing evidence on the expression and functional role of the inflammasome-caspase-1-IL-1β/IL-18 axis in kidney disease. We further provide a perspective on the potential roles of the inflammasomes in the pathogenesis of acute and chronic kidney diseases.