The influence of age on the clinical features and outcomes of anti-glomerular basement membrane disease.

摘要

To the Editor: We read with interest the contribution by Cui et al, who reported that older patients with anti-glomerular basement membrane (anti-GBM) disease had milder kidney damage and less pulmonary involvement, but did not specify a mechanism. We suggest a possible mechanism. According to a study by Fu et al, stimulation of Toll-like receptors (TLRs), a component of the innate immune system, can accentuate anti-GBM antibody-mediated nephritis. Recently, Summers et al showed that activation of TLR9, in particular, promotes nephritogenic immunity and glomerular leukocyte recruitment, exacerbating experimental crescentic glomerulonephritis. Innate and adaptive immune stimuli appear to synergistically activate several cytokines and chemokines that are essential for the development of kidney disease. Ito et al reported the pathogenic significance of IL-6 (interleukin 6) in anti-GBM disease, and Mulligan et al showed that inhibition of TNF-alpha (tumor necrosis factor alpha) or IL-1 attenuates kidney and lung injury caused by anti-GBM antibodies. In the study of Kim et al, TNF-alpha consistently was activated throughout anti-GBM disease progression, together with enhanced IL-1beta and IL-6 expression.