The inflammasome is a large, multiprotein complex that drives proinflammatory cytokine production in response to
infection and tissue injury. Pattern recognition receptors that are either membrane bound or cytoplasmic trigger
inflammasome assembly. These receptors sense danger signals including damage-associated molecular patterns and
pathogen-associated molecular patterns (DAMPS and PAMPS respectively). The best-characterized inflammasome is the
NLRP3 inflammasome. On assembly of the NLRP3 inflammasome, post-translational processing and secretion of
pro-inflammatory cytokines IL-1β and IL-18 occurs; in addition, cell death may be mediated via caspase-1. Intrinsic renal
cells express components of the inflammasome pathway. This is most prominent in tubular epithelial cells and, to a
lesser degree, in glomeruli. Several primary renal diseases and systemic diseases affecting the kidney are associated with
NLRP3 inflammasome/IL-1β/IL-18 axis activation. Most of the disorders studied have been acute inflammatory diseases.
The disease spectrum includes ureteric obstruction, ischaemia reperfusion injury, glomerulonephritis, sepsis, hypoxia,
glycerol-induced renal failure, and crystal nephropathy. In addition to mediating renal disease, the IL-1/ IL-18 axis may
also be responsible for development of CKD itself and its related complications, including vascular calcification and
sepsis. Experimental models using genetic deletions and/or receptor antagonists/antiserum against the NLRP3
inflammasome pathway have shown decreased severity of disease. As such, the inflammasome is an attractive
potential therapeutic target in a variety of renal diseases.