Kidney Disease and Gout: The Role of the Innate Immune System
William F. Finn*
Identifiers and Pagination:Year: 2016
Issue: Suppl 1: M3
First Page: 12
Last Page: 21
Publisher ID: TOUNJ-9-12
Article History:Received Date: 18/4/2015
Revision Received Date: 30/4/2015
Acceptance Date: 30/4/2015
Electronic publication date: 11/02/2016
Collection year: 2016
open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) (https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
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.