, Volume 387, Issue 10, pp 905-907
Date: 10 Aug 2014

Blocking innate immunity to slow the progression of chronic kidney disease

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Chronic inflammation is present in almost every biopsy of patients with chronic kidney disease. It is independent of the cause of kidney injury and can be detected in acute kidney failure and chronic kidney allograft nephropathy, autoimmune diseases like lupus nephritis or granulomatosis with polyangiitis, and even diabetic nephropathy. Chronic inflammation does not seem to be triggered by pathogens be it viruses, bacteria, or bacterial products (Leemans et al. 2014).

During the last few years, numerous endogenous ligands have been identified that can bind to damage-associated molecular patterns (DAMPs) and trigger inflammation by activating nuclear factor kappa b and secreting cytokines and chemokines (Leemans et al. 2014). The resulting kidney tissue damage is associated with the release of more endogenous ligands and, therefore, ends in a self-sustaining vicious circle. The idea of blocking a crucial molecule in the innate immunity pathway namely interleukin-1 receptor-associated kin