The clinical manifestations and consequence of acute and chronic gout are closely associated with the activation of the innate immune system, stimulation of the NLP3 inflammasome and secretion of interleukin-1β and interleukin-18 via caspace-1 activity. This leads to cytokine release and an inflammatory response. It is now clear that a similar involvement of the innate immune system occurs in many forms of acute and chronic kidney disease with accentuation of renal tubular injury and stimulation of tubulointerstitial fibrosis. The local and systemic activation of the innate immune system may help explain the close association of these conditions and provide a target for therapeutic interdiction.
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