Why does renal inflammation appear among many of the so-called noninflammatory kidney
diseases? Toll-like receptor research provides a surprising answer because activation of the
innate immune system involves pathogen-derived as well as nonpathogen-derived
immunostimulatory molecules; thus, metabolic, hemodynamic, toxic, or autoimmune forms of
tissue damage all can trigger an innate inflammatory response. Because receptor activation
is unable to eliminate the underlying drivers of these nonpathogen diseases, it becomes …