Korean Journal of Nephrology 2001;20(5):824-833.
원저 : 고뇨산성 신병증 발병 기전에서 대식세포 유주 억제 인자의 역할 (Original Articles : Involvement of Macrophage Migration Inhibitory Factor ( MIF ) in Experimental Uric Acid Nephropathy)
정시정(Shi Jung Chung),최성철(Sung Chul Choi),도정호(Jung Ho Do),김정아(Jung Ah Kim),윤수진(Soo Jin Yoon),이현희(Hyun Hee Lee),박진아(Jin Ah Park),한혁준(Hyeok Jun Han),이영기(Young Kee Lee),허우성(Woo Seong Huh),김대중(Dae Joong Kim),김윤구(Yoon Goo Kim)
Abstract
Chronic deposition of uric acid in the kidney can lead to progressive tubulointerstitial injury with granuloma formation. We hypothesized that uric acid crystal deposition may induce granuloma formation by stimulating local expression of macrophage migration inhibitory factor(MIF), which is a known mediator of delayed type hypersensitivity(DTH). A model of acute uric acid nephropathy was induced in rats by the administration of oxonic acid (an inhibitor of uricase) together with uric acid supplements. Kidney tissue examined at 35 days showed widespread tubulointerstitial damage with intratubular uric acid crystals deposition and granuloma formation. Tubules within the areas of granuloma showed a six-fold increase in MIF mRNA compared to uninvolved areas by in situ hybridization. Moreover, the areas of increased MIF mRNA expression correlated with sites of dense accumulation of macrophages and T cells. Control rats fed a normal diet had no discernible evidence of renal disease by routine light microscopy and minimal tubular expression of MIF mRNA and protein. These data suggest that intrarenal granulomas in urate nephropathy may be the consequence of a crystal induced DTH-like reaction mediated by MIF.
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