Involvement of Macrophage Migration Inhibitory Factor(MIF) in Experimental Uric Acid Nephropathy.
- Author:
Shi Jung CHUNG
1
;
Sung Chul CHOI
;
Jung Ho DO
;
Jung Ah KIM
;
Soo Jin YOON
;
Hyun Hee LEE
;
Jinah PARK
;
Hyeok Jun HAN
;
Young Kee LEE
;
Wooseong HUH
;
Dae Joong KIM
;
Yoon Goo KIM
;
Ha Young OH
;
Dong Jin OH
Author Information
1. Department of Internal Medicine, Samsung Medical Center, College of Medicine, Sungkyunkwan University, Seoul, Korea. ygkim@samsung.co.kr
- Publication Type:Original Article
- Keywords:
Macrophage migration inhibitory factor;
Uric acid;
Uric acid nephropathy
- MeSH:
Rats;
Animals
- From:Korean Journal of Nephrology
2001;20(5):824-833
- CountryRepublic of Korea
- Language:Korean
-
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.
